Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Tumor suppressor genes located on human chromosome 9 in the region 9p21. This gene is either deleted or mutated in a wide range of malignancies. (From Segen, Current Med Talk, 1995) Two alternatively spliced gene products are encoded by p16: CYCLIN-DEPENDENT KINASE INHIBITOR P16 and TUMOR SUPPRESSOR PROTEIN P14ARF.
A product of the p16 tumor suppressor gene (GENES, P16). It is also called INK4 or INK4A because it is the prototype member of the INK4 CYCLIN-DEPENDENT KINASE INHIBITORS. This protein is produced from the alpha mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced beta transcript, is TUMOR SUPPRESSOR PROTEIN P14ARF. Both p16 gene products have tumor suppressor functions.
A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.
An INK4 cyclin-dependent kinase inhibitor containing four ANKYRIN-LIKE REPEATS. INK4B is often inactivated by deletions, mutations, or hypermethylation in HEMATOLOGIC NEOPLASMS.
Genes that inhibit expression of the tumorigenic phenotype. They are normally involved in holding cellular growth in check. When tumor suppressor genes are inactivated or lost, a barrier to normal proliferation is removed and unregulated growth is possible.
Variation in a population's DNA sequence that is detected by determining alterations in the conformation of denatured DNA fragments. Denatured DNA fragments are allowed to renature under conditions that prevent the formation of double-stranded DNA and allow secondary structure to form in single stranded fragments. These fragments are then run through polyacrylamide gels to detect variations in the secondary structure that is manifested as an alteration in migration through the gels.
A potent inhibitor of CYCLIN-DEPENDENT KINASES in G1 PHASE and S PHASE. In humans, aberrant expression of p57 is associated with various NEOPLASMS as well as with BECKWITH-WIEDEMANN SYNDROME.
A specific pair of GROUP C CHROMSOMES of the human chromosome classification.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. They generally function as ENZYME ACTIVATORS that drive the CELL CYCLE through transitions between phases. A subset of cyclins may also function as transcriptional regulators.
A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
An E3 UBIQUITIN LIGASE that interacts with and inhibits TUMOR SUPPRESSOR PROTEIN P53. Its ability to ubiquitinate p53 is regulated by TUMOR SUPPRESSOR PROTEIN P14ARF.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Addition of methyl groups to DNA. DNA methyltransferases (DNA methylases) perform this reaction using S-ADENOSYLMETHIONINE as the methyl group donor.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A gene product of the p16 tumor suppressor gene (GENES, P16). It antagonizes the function of MDM2 PROTEIN (which regulates P53 TUMOR SUPPRESSOR PROTEIN by targeting it for degradation). p14ARF is produced from the beta mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced alpha transcript, is CYCLIN-DEPENDENT KINASE INHIBITOR P16. Both p16 gene products have tumor suppressor functions.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A genus of the family BACULOVIRIDAE, subfamily Eubaculovirinae, characterized by the formation of crystalline, polyhedral occlusion bodies in the host cell nucleus. The type species is Autographa californica nucleopolyhedrovirus.
A cell line derived from cultured tumor cells.
The decrease in the cell's ability to proliferate with the passing of time. Each cell is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences CELL DEATH via the process of APOPTOSIS.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
The loss of one allele at a specific locus, caused by a deletion mutation; or loss of a chromosome from a chromosome pair, resulting in abnormal HEMIZYGOSITY. It is detected when heterozygous markers for a locus appear monomorphic because one of the ALLELES was deleted.
Established cell cultures that have the potential to propagate indefinitely.
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
Cellular proteins encoded by the H-ras, K-ras and N-ras genes. The proteins have GTPase activity and are involved in signal transduction as monomeric GTP-binding proteins. Elevated levels of p21 c-ras have been associated with neoplasia. This enzyme was formerly listed as EC 3.6.1.47.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.
Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.
A family of non-enveloped viruses infecting mammals (MASTADENOVIRUS) and birds (AVIADENOVIRUS) or both (ATADENOVIRUS). Infections may be asymptomatic or result in a variety of diseases.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Areas of increased density of the dinucleotide sequence cytosine--phosphate diester--guanine. They form stretches of DNA several hundred to several thousand base pairs long. In humans there are about 45,000 CpG islands, mostly found at the 5' ends of genes. They are unmethylated except for those on the inactive X chromosome and some associated with imprinted genes.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
DNA present in neoplastic tissue.
Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.
Biochemical identification of mutational changes in a nucleotide sequence.
A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
The functional hereditary units of VIRUSES.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
Protein kinases that control cell cycle progression in all eukaryotes and require physical association with CYCLINS to achieve full enzymatic activity. Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumorigenesis.
A malignant epithelial tumor with a glandular organization.
Tumors or cancer of the SKIN.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.
Proteins which maintain the transcriptional quiescence of specific GENES or OPERONS. Classical repressor proteins are DNA-binding proteins that are normally bound to the OPERATOR REGION of an operon, or the ENHANCER SEQUENCES of a gene until a signal occurs that causes their release.
Formation of an acetyl derivative. (Stedman, 25th ed)
Product of the retinoblastoma tumor suppressor gene. It is a nuclear phosphoprotein hypothesized to normally act as an inhibitor of cell proliferation. Rb protein is absent in retinoblastoma cell lines. It also has been shown to form complexes with the adenovirus E1A protein, the SV40 T antigen, and the human papilloma virus E7 protein.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, Ki-ras, rasK) murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras genes have been detected in human, avian, murine, and non-vertebrate genomes. The closely related N-ras gene has been detected in human neuroblastoma and sarcoma cell lines. All genes of the family have a similar exon-intron structure and each encodes a p21 protein.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Tumors or cancer of the LUNG.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Proteins found in any species of virus.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
Molecular products metabolized and secreted by neoplastic tissue and characterized biochemically in cells or body fluids. They are indicators of tumor stage and grade as well as useful for monitoring responses to treatment and predicting recurrence. Many chemical groups are represented including hormones, antigens, amino and nucleic acids, enzymes, polyamines, and specific cell membrane proteins and lipids.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Tumors or cancer of the human BREAST.
Transport proteins that carry specific substances in the blood or across cell membranes.
Elements of limited time intervals, contributing to particular results or situations.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.

Expression of Bcl-2 protein is decreased in colorectal adenocarcinomas with microsatellite instability. (1/4420)

Bcl-2 is known to inhibit apoptosis and is thought to play a role in colorectal tumour development. Studies of the promoter region of bcl-2 have indicated the presence of a p53 responsive element which downregulates bcl-2 expression. Since p53 is commonly mutated in colorectal cancers, but rarely in those tumours showing microsatellite instability (MSI), the aim of this study was to examine the relationship of bcl-2 protein expression to MSI, as well as to other clinicopathological and molecular variables, in colorectal adenocarcinomas. Expression of bcl-2 was analysed by immunohistochemistry in 71 colorectal cancers which had been previously assigned to three classes depending upon their levels of MSI. MSI-high tumours demonstrated instability in three or more of six microsatellite markers tested, MSI-low tumours in one or two of six, and MSI-null in none of six. Bcl-2 expression in tumours was quantified independently by two pathologists and assigned to one of five categories, with respect to the number of cells which showed positive staining: 0, up to 5%; 1, 6-25%; 2, 26-50%; 3, 51-75%; and 4, > or =76%. Bcl-2 negative tumours were defined as those with a score of 0. Bcl-2 protein expression was tested for association with clinicopathological stage, differentiation level, tumour site, age, sex, survival, evidence of p53 inactivation and MSI level. A significant association was found between bcl-2 expression and patient survival (P = 0.012, Gehan Wilcoxon test). Further, a significant reciprocal relationship was found between bcl-2 expression and the presence of MSI (P = 0.012, Wilcoxon rank sum test). We conclude that bcl-2 expressing colorectal cancers are more likely to be MSI-null, and to be associated with improved patient survival.  (+info)

Comparative molecular genetic profiles of anaplastic astrocytomas/glioblastomas multiforme and their subsequent recurrences. (2/4420)

Malignant glial tumors (anaplastic astrocytomas and glioblastomas multiforme) arise mostly either from the progression of low grade precursor lesions or rapidly in a de novo fashion and contain distinct genetic alterations. There is, however, a third subset of malignant gliomas in which genetic lesions remain to be identified. Following surgical resection, all gliomas appear to have an inherent tendency to recur. Comparative molecular analysis of ten primary malignant gliomas (three anaplastic astrocytomas and seven glioblastomas multiforme) with their recurrences identified two distinct subgroups of recurrent tumors. In one group, primary tumors harbored genetic aberrations frequently associated with linear progression or de novo formation pathways of glial tumorigenesis and maintained their genetic profiles upon recurrence. In the other subset with no detectable known genetic mutations at first presentation, the recurrent tumors sustained specific abnormalities associated with pathways of linear progression or de novo formation. These included loss of genes on chromosomes 17 and 10, mutations in the p53 gene, homozygous deletion of the DMBTA1 and p16 and/ or p15 genes and amplification and/or overexpression of CDK4 and alpha form of the PDGF receptor. Recurrent tumors from both groups also displayed an abnormal expression profile of the metalloproteinase, gel A, and its inhibitor, TIMP-2, consistent with their highly invasive behavior. Delineation of the molecular differences between malignant glioblastomas and their subsequent recurrences may have important implications for the development of rational clinical approaches for this neoplasm that remains refractory to existing therapeutic modalities.  (+info)

Expression of vascular endothelial growth factor in human oral squamous cell carcinoma: its association with tumour progression and p53 gene status. (3/4420)

AIMS: To correlate vascular endothelial growth factor (VEGF) expression in oral squamous cell carcinoma with the clinicopathological characteristics and prognosis; and to assess whether p53 gene status is associated with VEGF expression in human cancers. METHODS: Tumour specimens from 45 patients with oral squamous cell carcinomas were examined. Expression of VEGF was determined using an immunohistochemical method, and a tumour was considered positive when more than 5% of the neoplastic cells showed VEGF immunoreactivity. The p53 gene status was screened using a polymerase chain reaction--single strand conformation polymorphism analysis. RESULTS: VEGF positive staining was detected in 19 (42.2%) of the 45 cases. VEGF immunoreactivity did not correlate with the histological degree of tumour differentiation, clinical stages, or lymph node metastasis. The patients with VEGF positive tumours had a significantly worse prognosis than those with VEGF negative tumours. The five year overall survival rate of the VEGF negative patients was 76.5%, as compared with 48.8% for the VEGF positive patients. No significant association between VEGF expression and the p53 gene status of the tumours was found. CONCLUSIONS: VEGF is a good prognostic indicator of the survival of patients with oral squamous cell carcinoma. The p53 gene status does not seem to be associated with VEGF expression in these cancers.  (+info)

Transcriptional regulation and induction of apoptosis: implications for the use of monomeric p53 variants in gene therapy. (4/4420)

The p53 tumour suppressor protein is a transcriptional activator, which can induce cell cycle arrest and apoptosis. p53 Gene mutations occur in more than 50% of all human tumours. Reintroduction of wild-type p53 but also of oligomerisation-independent p53 variants into tumour cells by gene transfer methods has been considered. We have investigated the biological properties of two carboxy-terminal deletion mutants of p53, p53 delta 300 (comprising amino acids 1-300) and p53 delta 326 (amino acids 1-326), to evaluate their potential deployment in gene therapy. Transactivation was measured in transiently transfected HeLa and SKBR3 cells. Both monomeric variants showed reduced activities compared with wild-type p53. Individual promoters were differently affected. In contrast to wild-type p53, monomeric variants were not able to induce apoptosis. We also provided wild-type p53 and p53 delta 326 with tetracycline-regulated promoters and stably introduced these constructs into Saos2 and SKBR3 cells. Upon induction, wild-type p53 expressing cells, but not p53 delta 326 expressing cells underwent apoptosis. Consistently, only wild-type p53 expressing cells accumulated p21/waf1/cip1 mRNA and protein and showed increased bax, Gadd45 and mdm2 mRNA. Neither wild-type p53 nor p53 delta 326 repressed the transcription of the IGF-1R gene in these cell lines. We conclude that the transactivation potential of monomeric, carboxy-terminally truncated p53 is not sufficient to cause induction of the endogenous target genes which trigger apoptosis.  (+info)

Multiple target sites of allelic imbalance on chromosome 17 in Barrett's oesophageal cancer. (5/4420)

Twelve Barrett's adenocarcinomas have been analysed for the occurrence of allelic imbalance (LOH) on chromosome 17 using 41 microsatellite markers. This study provides evidence for 13 minimal regions of LOH, six on 17p and seven on 17q. Four of these centre in the vicinity of the known tumour suppressor genes (TSGs) TP53 (17p13.1), NFI (17q11.2), BRCA1 (17q21.1), and a putative TSG (17p13.3). The tumours all displayed relatively small regions of LOH (1-10 cM), and in several tumours extensive regions of LOH were detected. One tumour displayed only two very small regions of LOH; 17p11.2 and 17p13.1. The frequency of allelic imbalance has been calculated based on the LOH encompassing only one minimal region, and based on all the LOH observations. By both evaluations the highest LOH frequencies were found for regions II (p53), III (17p13.1 centromeric to p53), IV (17p12), V (17p11.2) and VII (NF1, 17q11.2). Our data supports the existence of multiple TSGs on chromosome 17 and challenges the view that p53 is the sole target of LOH on 17p in Barrett's adenocarcinoma.  (+info)

Correlation between the status of the p53 gene and survival in patients with stage I non-small cell lung carcinoma. (6/4420)

The association of p53 abnormalities with the prognosis of patients with non-small cell lung carcinoma (NSCLC) has been extensively investigated to date, however, this association is still controversial. Therefore, we investigated the prognostic significance of p53 mutations through exons 2 to 11 and p53 protein expression in 103 cases of stage I NSCLC. p53 mutations were detected in 49 of 103 (48%) tumors. Two separate mutations were detected in four tumors giving a total of 53 unique mutations in 49 tumors. Ten (19%) of mutations occurred outside exons 5-8. Positive immunohistochemical staining of p53 protein was detected in 41 of 103 (40%) tumors. The concordance rate between mutations and protein overexpression was only 69%. p53 mutations, but not expression, were significantly associated with a shortened survival of patients (P<0.001). Furthermore, we investigated the correlation between the types of p53 mutations and prognosis. p53 missense mutations rather than null mutations were associated with poor prognosis (P < 0.001 in missense mutations and P=0.243 in null mutations). These results indicated that p53 mutations, in particular missense mutations, rather than p53 expression could be a useful molecular marker for the prognosis of patients with surgically resected stage I NSCLC.  (+info)

Estrogen-dependent and independent activation of the P1 promoter of the p53 gene in transiently transfected breast cancer cells. (7/4420)

Loss of p53 function by mutational inactivation is the most common marker of the cancerous phenotype. Previous studies from our laboratory have demonstrated 17 beta estradiol (E2) induction of p53 protein expression in breast cancer cells. Although direct effects of E2 on the expression of p53 gene are not known, the steroid is a potent regulator of c-Myc transcription. In the present studies, we have examined the ability of E2 and antiestrogens to regulate the P1 promoter of the p53 gene which contains a c-Myc responsive element. Estrogen receptor (ER)-positive T47D and MCF-7 cells were transiently transfected with the P1CAT reporter plasmid and levels of CAT activity in response to serum, E2 and antiestrogens were monitored. Factors in serum were noted to be the dominant inducers of chloramphenicol acetyltransferase (CAT) expression in MCF-7 cells. The levels of CAT were drastically reduced when cells were maintained in serum free medium (SFM). However, a subtle ER-mediated induction of CAT expression was detectable when MCF-7 cells, cultured in SFM, were treated with E2. In serum-stimulated T47D cells, the CAT expression was minimal. The full ER antagonist, ICI 182 780 (ICI) had no effect. Treatment with E2 or 4-hydroxy tamoxifen (OHT) resulted in P1CAT induction; OHT was more effective than E2. Consistent with c-Myc regulation of the P1 promoter, E2 stimulated endogenous c-Myc in both cell lines. Two forms of c-Myc were expressed independent of E2 stimuli. The expression of a third more rapidly migrating form was E2-dependent and ER-mediated since it was blocked by the full ER antagonist, ICI, but not by the ER agonist/antagonist OHT. These data demonstrate both ER-mediated and ER-independent regulation of c-Myc and the P1 promoter of the p53 gene, and show differential effects of the two classes of antiestrogens in their ability to induce the P1 promoter of the p53 gene in breast cancer cells.  (+info)

Adenovirus mediated p53 tumour suppressor gene therapy for human gastric cancer cells in vitro and in vivo. (8/4420)

BACKGROUND/AIMS: Gastric cancer is one of the most prevalent forms of cancer in East Asia. Point mutation of the p53 gene has been reported in more than 60% of cases of gastric cancer and can lead to genetic instability and uncontrolled cell proliferation. The purpose of this investigation was to evaluate the potential of p53 gene therapy for gastric cancer. METHODS: The responses of human gastric cancer cell lines, MKN1, MKN7, MKN28, MKN45, and TMK-1, to recombinant adenoviruses encoding wild type p53 (AdCAp53) were analysed in vitro. The efficacy of the AdCAp53 treatment for MKN1 and MKN45 subcutaneous tumours in nude mice was assessed in vivo. RESULTS: p53-specific growth inhibition was observed in vitro in two of four gastric cancer cell lines with mutated p53, but not in the wild type p53 cell line. The mechanism of the killing of gastric cancer cells by AdCAp53 was found, by flow cytometric analysis and detection of DNA fragmentation, to be apoptosis. In vivo studies showed that the growth of subcutaneous tumours of p53 mutant MKN1 cells was significantly inhibited by direct injection of AdCAp53, but no significant growth inhibition was detected in the growth of p53 wild type MKN45 tumours. CONCLUSIONS: Adenovirus mediated reintroduction of wild type p53 is a potential clinical utility in gene therapy for gastric cancers.  (+info)

p53 is a tumor suppressor gene that encodes a protein responsible for controlling cell growth and division. The p53 protein plays a crucial role in preventing the development of cancer by regulating the cell cycle and activating DNA repair processes when genetic damage is detected. If the damage is too severe to be repaired, p53 can trigger apoptosis, or programmed cell death, to prevent the propagation of potentially cancerous cells. Mutations in the TP53 gene, which encodes the p53 protein, are among the most common genetic alterations found in human cancers and are often associated with a poor prognosis.

Tumor suppressor protein p53, also known as p53 or tumor protein p53, is a nuclear phosphoprotein that plays a crucial role in preventing cancer development and maintaining genomic stability. It does so by regulating the cell cycle and acting as a transcription factor for various genes involved in apoptosis (programmed cell death), DNA repair, and cell senescence (permanent cell growth arrest).

In response to cellular stress, such as DNA damage or oncogene activation, p53 becomes activated and accumulates in the nucleus. Activated p53 can then bind to specific DNA sequences and promote the transcription of target genes that help prevent the proliferation of potentially cancerous cells. These targets include genes involved in cell cycle arrest (e.g., CDKN1A/p21), apoptosis (e.g., BAX, PUMA), and DNA repair (e.g., GADD45).

Mutations in the TP53 gene, which encodes p53, are among the most common genetic alterations found in human cancers. These mutations often lead to a loss or reduction of p53's tumor suppressive functions, allowing cancer cells to proliferate uncontrollably and evade apoptosis. As a result, p53 has been referred to as "the guardian of the genome" due to its essential role in preventing tumorigenesis.

p16, also known as CDKN2A, is a tumor suppressor gene that encodes the protein p16INK4a. This protein plays a crucial role in regulating the cell cycle by inhibiting the activity of cyclin-dependent kinases (CDKs) 4 and 6, which are essential for the progression from G1 to S phase.

The p16 gene is located on chromosome 9p21 and is often inactivated or deleted in various types of cancer, including lung, breast, and head and neck cancers. Inactivation of the p16 gene leads to uncontrolled cell growth and division, which can contribute to tumor development and progression.

Therefore, the p16 gene is an important tumor suppressor gene that helps prevent cancer by regulating cell growth and division.

Cyclin-Dependent Kinase Inhibitor p16, also known as CDKN2A or INK4a, is a protein that regulates the cell cycle. It functions as an inhibitor of cyclin-dependent kinases (CDKs) 4 and 6, which are enzymes that play a crucial role in regulating the progression of the cell cycle.

The p16 protein is produced in response to various signals, including DNA damage and oncogene activation, and its main function is to prevent the phosphorylation and activation of the retinoblastoma protein (pRb) by CDK4/6. When pRb is not phosphorylated, it binds to and inhibits the E2F transcription factor, which results in the suppression of genes required for cell cycle progression.

Therefore, p16 acts as a tumor suppressor protein by preventing the uncontrolled proliferation of cells that can lead to cancer. Mutations or deletions in the CDKN2A gene, which encodes the p16 protein, have been found in many types of human cancers, including lung, breast, and head and neck cancers.

Cyclin-dependent kinase inhibitor p21, also known as CDKN1A or p21/WAF1/CIP1, is a protein that regulates the cell cycle. It inhibits the activity of cyclin-dependent kinases (CDKs), which are enzymes that play crucial roles in controlling the progression of the cell cycle.

The binding of p21 to CDKs prevents the phosphorylation and activation of downstream targets, leading to cell cycle arrest. This protein is transcriptionally activated by tumor suppressor protein p53 in response to DNA damage or other stress signals, and it functions as an important mediator of p53-dependent growth arrest.

By inhibiting CDKs, p21 helps to ensure that cells do not proceed through the cell cycle until damaged DNA has been repaired, thereby preventing the propagation of potentially harmful mutations. Additionally, p21 has been implicated in other cellular processes such as apoptosis, differentiation, and senescence. Dysregulation of p21 has been associated with various human diseases, including cancer.

Cyclin-Dependent Kinase Inhibitor p15, also known as CDKN2B or INK4b, is a protein that regulates the cell cycle. It inhibits the activity of cyclin-dependent kinases (CDKs), specifically the CDK4 and CDK6 complexes with cyclin D, which play a crucial role in regulating the progression of the cell cycle from the G1 phase to the S phase.

The p15 protein is encoded by the CDKN2B gene, which is located on human chromosome 9p21. The expression of the CDKN2B gene is induced by various signals, including DNA damage and differentiation signals, leading to the inhibition of CDK4/6-cyclin D complexes and cell cycle arrest in the G1 phase. This provides an essential mechanism for preventing cells with damaged DNA from entering the S phase and undergoing DNA replication, thereby ensuring genomic stability and preventing tumorigenesis.

Mutations or deletions of the CDKN2B gene have been implicated in various human cancers, including gliomas, melanomas, and leukemias, suggesting that the loss of p15 function may contribute to tumor development and progression.

Tumor suppressor genes are a type of gene that helps to regulate and prevent cells from growing and dividing too rapidly or in an uncontrolled manner. They play a critical role in preventing the formation of tumors and cancer. When functioning properly, tumor suppressor genes help to repair damaged DNA, control the cell cycle, and trigger programmed cell death (apoptosis) when necessary. However, when these genes are mutated or altered, they can lose their ability to function correctly, leading to uncontrolled cell growth and the development of tumors. Examples of tumor suppressor genes include TP53, BRCA1, and BRCA2.

Single-Stranded Conformational Polymorphism (SSCP) is not a medical condition but rather a laboratory technique used in molecular biology and genetics. It refers to the phenomenon where a single-stranded DNA or RNA molecule can adopt different conformations or shapes based on its nucleotide sequence, even if the difference in the sequence is as small as a single base pair change. This property is used in SSCP analysis to detect mutations or variations in DNA or RNA sequences.

In SSCP analysis, the denatured single-stranded DNA or RNA sample is subjected to electrophoresis on a non-denaturing polyacrylamide gel. The different conformations of the single-stranded molecules migrate at different rates in the gel, creating multiple bands that can be visualized by staining or other detection methods. The presence of additional bands or shifts in band patterns can indicate the presence of a sequence variant or mutation.

SSCP analysis is often used as a screening tool for genetic diseases, cancer, and infectious diseases to identify genetic variations associated with these conditions. However, it has largely been replaced by more sensitive and accurate methods such as next-generation sequencing.

Cyclin-dependent kinase inhibitor p57, also known as CDKN1C or p57KIP2, is a protein that regulates the cell cycle and acts as a tumor suppressor. It inhibits the activity of cyclin-dependent kinases (CDKs), which are enzymes that play crucial roles in regulating the cell cycle and transitioning from one phase to another.

The p57 protein is encoded by the CDKN1C gene, which is located on chromosome 11p15.5. This region is known as an imprinted gene cluster, meaning that only one copy of the gene is active, depending on whether it is inherited from the mother or father. In the case of p57, the paternal allele is usually silenced, and only the maternal allele is expressed.

Mutations in the CDKN1C gene can lead to several developmental disorders, including Beckwith-Wiedemann syndrome (BWS), a condition characterized by overgrowth, abdominal wall defects, and an increased risk of childhood tumors. Loss of function mutations in CDKN1C have also been associated with an increased risk of cancer, particularly Wilms' tumor, a type of kidney cancer that typically affects children.

In summary, cyclin-dependent kinase inhibitor p57 is a protein that regulates the cell cycle and acts as a tumor suppressor by inhibiting the activity of CDKs. Mutations in the CDKN1C gene can lead to developmental disorders and an increased risk of cancer.

Human chromosome pair 9 consists of two rod-shaped structures present in the nucleus of each cell of the human body. Each member of the pair contains thousands of genes and other genetic material, encoded in the form of DNA molecules. The two chromosomes in a pair are identical or very similar to each other in terms of their size, shape, and genetic makeup.

Chromosome 9 is one of the autosomal chromosomes, meaning that it is not a sex chromosome (X or Y) and is present in two copies in all cells of the body, regardless of sex. Chromosome 9 is a medium-sized chromosome, and it is estimated to contain around 135 million base pairs of DNA and approximately 1200 genes.

Chromosome 9 contains several important genes that are associated with various human traits and diseases. For example, mutations in the gene that encodes the protein APOE on chromosome 9 have been linked to an increased risk of developing Alzheimer's disease. Additionally, variations in the gene that encodes the protein EGFR on chromosome 9 have been associated with an increased risk of developing certain types of cancer.

Overall, human chromosome pair 9 plays a critical role in the development and function of the human body, and variations in its genetic makeup can contribute to a wide range of traits and diseases.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Tumor suppressor proteins are a type of regulatory protein that helps control the cell cycle and prevent cells from dividing and growing in an uncontrolled manner. They work to inhibit tumor growth by preventing the formation of tumors or slowing down their progression. These proteins can repair damaged DNA, regulate gene expression, and initiate programmed cell death (apoptosis) if the damage is too severe for repair.

Mutations in tumor suppressor genes, which provide the code for these proteins, can lead to a decrease or loss of function in the resulting protein. This can result in uncontrolled cell growth and division, leading to the formation of tumors and cancer. Examples of tumor suppressor proteins include p53, Rb (retinoblastoma), and BRCA1/2.

Cyclins are a family of regulatory proteins that play a crucial role in the cell cycle, which is the series of events that take place as a cell grows, divides, and produces two daughter cells. They are called cyclins because their levels fluctuate or cycle during the different stages of the cell cycle.

Cyclins function as subunits of serine/threonine protein kinase complexes, forming an active enzyme that adds phosphate groups to other proteins, thereby modifying their activity. This post-translational modification is a critical mechanism for controlling various cellular processes, including the regulation of the cell cycle.

There are several types of cyclins (A, B, D, and E), each of which is active during specific phases of the cell cycle:

1. Cyclin D: Expressed in the G1 phase, it helps to initiate the cell cycle by activating cyclin-dependent kinases (CDKs) that promote progression through the G1 restriction point.
2. Cyclin E: Active during late G1 and early S phases, it forms a complex with CDK2 to regulate the transition from G1 to S phase, where DNA replication occurs.
3. Cyclin A: Expressed in the S and G2 phases, it associates with both CDK2 and CDK1 to control the progression through the S and G2 phases and entry into mitosis (M phase).
4. Cyclin B: Active during late G2 and M phases, it partners with CDK1 to regulate the onset of mitosis by controlling the breakdown of the nuclear envelope, chromosome condensation, and spindle formation.

The activity of cyclins is tightly controlled through several mechanisms, including transcriptional regulation, protein degradation, and phosphorylation/dephosphorylation events. Dysregulation of cyclin expression or function can lead to uncontrolled cell growth and proliferation, which are hallmarks of cancer.

Gene deletion is a type of mutation where a segment of DNA, containing one or more genes, is permanently lost or removed from a chromosome. This can occur due to various genetic mechanisms such as homologous recombination, non-homologous end joining, or other types of genomic rearrangements.

The deletion of a gene can have varying effects on the organism, depending on the function of the deleted gene and its importance for normal physiological processes. If the deleted gene is essential for survival, the deletion may result in embryonic lethality or developmental abnormalities. However, if the gene is non-essential or has redundant functions, the deletion may not have any noticeable effects on the organism's phenotype.

Gene deletions can also be used as a tool in genetic research to study the function of specific genes and their role in various biological processes. For example, researchers may use gene deletion techniques to create genetically modified animal models to investigate the impact of gene deletion on disease progression or development.

Promoter regions in genetics refer to specific DNA sequences located near the transcription start site of a gene. They serve as binding sites for RNA polymerase and various transcription factors that regulate the initiation of gene transcription. These regulatory elements help control the rate of transcription and, therefore, the level of gene expression. Promoter regions can be composed of different types of sequences, such as the TATA box and CAAT box, and their organization and composition can vary between different genes and species.

Proto-oncogene proteins, such as c-MDM2, are normal cellular proteins that play crucial roles in regulating various cellular processes, including cell growth, differentiation, and apoptosis (programmed cell death). When these genes undergo mutations or are overexpressed, they can become oncogenes, which contribute to the development of cancer.

The c-MDM2 protein is a key regulator of the cell cycle and is involved in the negative regulation of the tumor suppressor protein p53. Under normal conditions, p53 helps prevent the formation of tumors by inducing cell cycle arrest or apoptosis in response to DNA damage or other stress signals. However, when c-MDM2 is overexpressed or mutated, it can bind and inhibit p53, leading to uncontrolled cell growth and increased risk of cancer development.

In summary, proto-oncogene proteins like c-MDM2 are important regulators of normal cellular processes, but when they become dysregulated through mutations or overexpression, they can contribute to the formation of tumors and cancer progression.

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

Polymerase Chain Reaction (PCR) is a laboratory technique used to amplify specific regions of DNA. It enables the production of thousands to millions of copies of a particular DNA sequence in a rapid and efficient manner, making it an essential tool in various fields such as molecular biology, medical diagnostics, forensic science, and research.

The PCR process involves repeated cycles of heating and cooling to separate the DNA strands, allow primers (short sequences of single-stranded DNA) to attach to the target regions, and extend these primers using an enzyme called Taq polymerase, resulting in the exponential amplification of the desired DNA segment.

In a medical context, PCR is often used for detecting and quantifying specific pathogens (viruses, bacteria, fungi, or parasites) in clinical samples, identifying genetic mutations or polymorphisms associated with diseases, monitoring disease progression, and evaluating treatment effectiveness.

DNA methylation is a process by which methyl groups (-CH3) are added to the cytosine ring of DNA molecules, often at the 5' position of cytospine phosphate-deoxyguanosine (CpG) dinucleotides. This modification is catalyzed by DNA methyltransferase enzymes and results in the formation of 5-methylcytosine.

DNA methylation plays a crucial role in the regulation of gene expression, genomic imprinting, X chromosome inactivation, and suppression of transposable elements. Abnormal DNA methylation patterns have been associated with various diseases, including cancer, where tumor suppressor genes are often silenced by promoter methylation.

In summary, DNA methylation is a fundamental epigenetic modification that influences gene expression and genome stability, and its dysregulation has important implications for human health and disease.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

p14ARF is a tumor suppressor protein that plays a crucial role in regulating the cell cycle and preventing uncontrolled cell growth, which can lead to cancer. It is encoded by the CDKN2A gene located on chromosome 9p21.3. The p14ARF protein functions by binding to and inhibiting the activity of MDM2, a negative regulator of the tumor suppressor protein p53. By inhibiting MDM2, p14ARF promotes the stabilization and activation of p53, leading to cell cycle arrest or apoptosis in response to oncogenic signals or DNA damage. Mutations or deletions in the CDKN2A gene can result in the loss of p14ARF function, contributing to tumorigenesis.

Nuclear proteins are a category of proteins that are primarily found in the nucleus of a eukaryotic cell. They play crucial roles in various nuclear functions, such as DNA replication, transcription, repair, and RNA processing. This group includes structural proteins like lamins, which form the nuclear lamina, and regulatory proteins, such as histones and transcription factors, that are involved in gene expression. Nuclear localization signals (NLS) often help target these proteins to the nucleus by interacting with importin proteins during active transport across the nuclear membrane.

Cyclin-Dependent Kinase Inhibitor p27, also known as CDKN1B or p27Kip1, is a protein that regulates the cell cycle. It inhibits the activity of certain cyclin-dependent kinases (CDKs), which are enzymes that play key roles in regulating the progression of the cell cycle.

The cell cycle is a series of events that cells undergo as they grow and divide. Cyclins and CDKs help to control the different stages of the cell cycle by activating and deactivating various proteins at specific times. The p27 protein acts as a brake on the cell cycle, preventing cells from dividing too quickly or abnormally.

When p27 binds to a CDK-cyclin complex, it prevents the complex from phosphorylating its target proteins, which are necessary for the progression of the cell cycle. By inhibiting CDK activity, p27 helps to ensure that cells divide only when the proper conditions are met.

Mutations in the CDKN1B gene, which encodes p27, have been associated with several types of cancer, including breast, lung, and prostate cancer. These mutations can lead to decreased levels of p27 or impaired function, allowing cells to divide uncontrollably and form tumors.

Cell division is the process by which a single eukaryotic cell (a cell with a true nucleus) divides into two identical daughter cells. This complex process involves several stages, including replication of DNA, separation of chromosomes, and division of the cytoplasm. There are two main types of cell division: mitosis and meiosis.

Mitosis is the type of cell division that results in two genetically identical daughter cells. It is a fundamental process for growth, development, and tissue repair in multicellular organisms. The stages of mitosis include prophase, prometaphase, metaphase, anaphase, and telophase, followed by cytokinesis, which divides the cytoplasm.

Meiosis, on the other hand, is a type of cell division that occurs in the gonads (ovaries and testes) during the production of gametes (sex cells). Meiosis results in four genetically unique daughter cells, each with half the number of chromosomes as the parent cell. This process is essential for sexual reproduction and genetic diversity. The stages of meiosis include meiosis I and meiosis II, which are further divided into prophase, prometaphase, metaphase, anaphase, and telophase.

In summary, cell division is the process by which a single cell divides into two daughter cells, either through mitosis or meiosis. This process is critical for growth, development, tissue repair, and sexual reproduction in multicellular organisms.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Neoplastic gene expression regulation refers to the processes that control the production of proteins and other molecules from genes in neoplastic cells, or cells that are part of a tumor or cancer. In a normal cell, gene expression is tightly regulated to ensure that the right genes are turned on or off at the right time. However, in cancer cells, this regulation can be disrupted, leading to the overexpression or underexpression of certain genes.

Neoplastic gene expression regulation can be affected by a variety of factors, including genetic mutations, epigenetic changes, and signals from the tumor microenvironment. These changes can lead to the activation of oncogenes (genes that promote cancer growth and development) or the inactivation of tumor suppressor genes (genes that prevent cancer).

Understanding neoplastic gene expression regulation is important for developing new therapies for cancer, as targeting specific genes or pathways involved in this process can help to inhibit cancer growth and progression.

The cell cycle is a series of events that take place in a cell leading to its division and duplication. It consists of four main phases: G1 phase, S phase, G2 phase, and M phase.

During the G1 phase, the cell grows in size and synthesizes mRNA and proteins in preparation for DNA replication. In the S phase, the cell's DNA is copied, resulting in two complete sets of chromosomes. During the G2 phase, the cell continues to grow and produces more proteins and organelles necessary for cell division.

The M phase is the final stage of the cell cycle and consists of mitosis (nuclear division) and cytokinesis (cytoplasmic division). Mitosis results in two genetically identical daughter nuclei, while cytokinesis divides the cytoplasm and creates two separate daughter cells.

The cell cycle is regulated by various checkpoints that ensure the proper completion of each phase before progressing to the next. These checkpoints help prevent errors in DNA replication and division, which can lead to mutations and cancer.

Cell cycle proteins are a group of regulatory proteins that control the progression of the cell cycle, which is the series of events that take place in a eukaryotic cell leading to its division and duplication. These proteins can be classified into several categories based on their functions during different stages of the cell cycle.

The major groups of cell cycle proteins include:

1. Cyclin-dependent kinases (CDKs): CDKs are serine/threonine protein kinases that regulate key transitions in the cell cycle. They require binding to a regulatory subunit called cyclin to become active. Different CDK-cyclin complexes are activated at different stages of the cell cycle.
2. Cyclins: Cyclins are a family of regulatory proteins that bind and activate CDKs. Their levels fluctuate throughout the cell cycle, with specific cyclins expressed during particular phases. For example, cyclin D is important for the G1 to S phase transition, while cyclin B is required for the G2 to M phase transition.
3. CDK inhibitors (CKIs): CKIs are regulatory proteins that bind to and inhibit CDKs, thereby preventing their activation. CKIs can be divided into two main families: the INK4 family and the Cip/Kip family. INK4 family members specifically inhibit CDK4 and CDK6, while Cip/Kip family members inhibit a broader range of CDKs.
4. Anaphase-promoting complex/cyclosome (APC/C): APC/C is an E3 ubiquitin ligase that targets specific proteins for degradation by the 26S proteasome. During the cell cycle, APC/C regulates the metaphase to anaphase transition and the exit from mitosis by targeting securin and cyclin B for degradation.
5. Other regulatory proteins: Several other proteins play crucial roles in regulating the cell cycle, such as p53, a transcription factor that responds to DNA damage and arrests the cell cycle, and the polo-like kinases (PLKs), which are involved in various aspects of mitosis.

Overall, cell cycle proteins work together to ensure the proper progression of the cell cycle, maintain genomic stability, and prevent uncontrolled cell growth, which can lead to cancer.

Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.

A nucleopolyhedrovirus (NPV) is a type of large, complex DNA virus that infects insects, particularly members of the order Lepidoptera (moths and butterflies). NPVs are characterized by their ability to produce multiple virions within a single polyhedral occlusion body, which provides protection for the virions in the environment and facilitates their transmission between hosts.

NPVs replicate in the nucleus of infected cells, where they induce the production of large quantities of viral proteins that ultimately lead to the lysis of the host cell. The virions are then released and can infect other cells or be transmitted to other insects. NPVs are important pathogens of many agricultural pests, and some species have been developed as biological control agents for use in integrated pest management programs.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Cellular aging, also known as cellular senescence, is a natural process that occurs as cells divide and grow older. Over time, cells accumulate damage to their DNA, proteins, and lipids due to various factors such as genetic mutations, oxidative stress, and epigenetic changes. This damage can impair the cell's ability to function properly and can lead to changes associated with aging, such as decreased tissue repair and regeneration, increased inflammation, and increased risk of age-related diseases.

Cellular aging is characterized by several features, including:

1. Shortened telomeres: Telomeres are the protective caps on the ends of chromosomes that shorten each time a cell divides. When telomeres become too short, the cell can no longer divide and becomes senescent or dies.
2. Epigenetic changes: Epigenetic modifications refer to chemical changes to DNA and histone proteins that affect gene expression without changing the underlying genetic code. As cells age, they accumulate epigenetic changes that can alter gene expression and contribute to cellular aging.
3. Oxidative stress: Reactive oxygen species (ROS) are byproducts of cellular metabolism that can damage DNA, proteins, and lipids. Accumulated ROS over time can lead to oxidative stress, which is associated with cellular aging.
4. Inflammation: Senescent cells produce pro-inflammatory cytokines, chemokines, and matrix metalloproteinases that contribute to a low-grade inflammation known as inflammaging. This chronic inflammation can lead to tissue damage and increase the risk of age-related diseases.
5. Genomic instability: DNA damage accumulates with age, leading to genomic instability and an increased risk of mutations and cancer.

Understanding cellular aging is crucial for developing interventions that can delay or prevent age-related diseases and improve healthy lifespan.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Gene expression is the process by which the information encoded in a gene is used to synthesize a functional gene product, such as a protein or RNA molecule. This process involves several steps: transcription, RNA processing, and translation. During transcription, the genetic information in DNA is copied into a complementary RNA molecule, known as messenger RNA (mRNA). The mRNA then undergoes RNA processing, which includes adding a cap and tail to the mRNA and splicing out non-coding regions called introns. The resulting mature mRNA is then translated into a protein on ribosomes in the cytoplasm through the process of translation.

The regulation of gene expression is a complex and highly controlled process that allows cells to respond to changes in their environment, such as growth factors, hormones, and stress signals. This regulation can occur at various stages of gene expression, including transcriptional activation or repression, RNA processing, mRNA stability, and translation. Dysregulation of gene expression has been implicated in many diseases, including cancer, genetic disorders, and neurological conditions.

Transfection is a term used in molecular biology that refers to the process of deliberately introducing foreign genetic material (DNA, RNA or artificial gene constructs) into cells. This is typically done using chemical or physical methods, such as lipofection or electroporation. Transfection is widely used in research and medical settings for various purposes, including studying gene function, producing proteins, developing gene therapies, and creating genetically modified organisms. It's important to note that transfection is different from transduction, which is the process of introducing genetic material into cells using viruses as vectors.

Exons are the coding regions of DNA that remain in the mature, processed mRNA after the removal of non-coding intronic sequences during RNA splicing. These exons contain the information necessary to encode proteins, as they specify the sequence of amino acids within a polypeptide chain. The arrangement and order of exons can vary between different genes and even between different versions of the same gene (alternative splicing), allowing for the generation of multiple protein isoforms from a single gene. This complexity in exon structure and usage significantly contributes to the diversity and functionality of the proteome.

Proto-oncogene proteins are normal cellular proteins that play crucial roles in various cellular processes, such as signal transduction, cell cycle regulation, and apoptosis (programmed cell death). They are involved in the regulation of cell growth, differentiation, and survival under physiological conditions.

When proto-oncogene proteins undergo mutations or aberrations in their expression levels, they can transform into oncogenic forms, leading to uncontrolled cell growth and division. These altered proteins are then referred to as oncogene products or oncoproteins. Oncogenic mutations can occur due to various factors, including genetic predisposition, environmental exposures, and aging.

Examples of proto-oncogene proteins include:

1. Ras proteins: Involved in signal transduction pathways that regulate cell growth and differentiation. Activating mutations in Ras genes are found in various human cancers.
2. Myc proteins: Regulate gene expression related to cell cycle progression, apoptosis, and metabolism. Overexpression of Myc proteins is associated with several types of cancer.
3. EGFR (Epidermal Growth Factor Receptor): A transmembrane receptor tyrosine kinase that regulates cell proliferation, survival, and differentiation. Mutations or overexpression of EGFR are linked to various malignancies, such as lung cancer and glioblastoma.
4. Src family kinases: Intracellular tyrosine kinases that regulate signal transduction pathways involved in cell proliferation, survival, and migration. Dysregulation of Src family kinases is implicated in several types of cancer.
5. Abl kinases: Cytoplasmic tyrosine kinases that regulate various cellular processes, including cell growth, differentiation, and stress responses. Aberrant activation of Abl kinases, as seen in chronic myelogenous leukemia (CML), leads to uncontrolled cell proliferation.

Understanding the roles of proto-oncogene proteins and their dysregulation in cancer development is essential for developing targeted cancer therapies that aim to inhibit or modulate these aberrant signaling pathways.

Loss of Heterozygosity (LOH) is a term used in genetics to describe the loss of one copy of a gene or a segment of a chromosome, where there was previously a pair of different genes or chromosomal segments (heterozygous). This can occur due to various genetic events such as mutation, deletion, or mitotic recombination.

LOH is often associated with the development of cancer, as it can lead to the loss of tumor suppressor genes, which normally help to regulate cell growth and division. When both copies of a tumor suppressor gene are lost or inactivated, it can result in uncontrolled cell growth and the formation of a tumor.

In medical terms, LOH is used as a biomarker for cancer susceptibility, progression, and prognosis. It can also be used to identify individuals who may be at increased risk for certain types of cancer, or to monitor patients for signs of cancer recurrence.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Proto-oncogene proteins c-bcl-2 are a group of proteins that play a role in regulating cell death (apoptosis). The c-bcl-2 gene produces one of these proteins, which helps to prevent cells from undergoing apoptosis. This protein is located on the membrane of mitochondria and endoplasmic reticulum and it can inhibit the release of cytochrome c, a key player in the activation of caspases, which are enzymes that trigger apoptosis.

In normal cells, the regulation of c-bcl-2 protein helps to maintain a balance between cell proliferation and cell death, ensuring proper tissue homeostasis. However, when the c-bcl-2 gene is mutated or its expression is dysregulated, it can contribute to cancer development by allowing cancer cells to survive and proliferate. High levels of c-bcl-2 protein have been found in many types of cancer, including leukemia, lymphoma, and carcinomas, and are often associated with a poor prognosis.

Transcriptional activation is the process by which a cell increases the rate of transcription of specific genes from DNA to RNA. This process is tightly regulated and plays a crucial role in various biological processes, including development, differentiation, and response to environmental stimuli.

Transcriptional activation occurs when transcription factors (proteins that bind to specific DNA sequences) interact with the promoter region of a gene and recruit co-activator proteins. These co-activators help to remodel the chromatin structure around the gene, making it more accessible for the transcription machinery to bind and initiate transcription.

Transcriptional activation can be regulated at multiple levels, including the availability and activity of transcription factors, the modification of histone proteins, and the recruitment of co-activators or co-repressors. Dysregulation of transcriptional activation has been implicated in various diseases, including cancer and genetic disorders.

DNA-binding proteins are a type of protein that have the ability to bind to DNA (deoxyribonucleic acid), the genetic material of organisms. These proteins play crucial roles in various biological processes, such as regulation of gene expression, DNA replication, repair and recombination.

The binding of DNA-binding proteins to specific DNA sequences is mediated by non-covalent interactions, including electrostatic, hydrogen bonding, and van der Waals forces. The specificity of binding is determined by the recognition of particular nucleotide sequences or structural features of the DNA molecule.

DNA-binding proteins can be classified into several categories based on their structure and function, such as transcription factors, histones, and restriction enzymes. Transcription factors are a major class of DNA-binding proteins that regulate gene expression by binding to specific DNA sequences in the promoter region of genes and recruiting other proteins to modulate transcription. Histones are DNA-binding proteins that package DNA into nucleosomes, the basic unit of chromatin structure. Restriction enzymes are DNA-binding proteins that recognize and cleave specific DNA sequences, and are widely used in molecular biology research and biotechnology applications.

BCL-2-associated X protein, often abbreviated as BAX, is a type of protein belonging to the BCL-2 family. The BCL-2 family of proteins plays a crucial role in regulating programmed cell death, also known as apoptosis. Specifically, BAX is a pro-apoptotic protein, which means that it promotes cell death.

BAX is encoded by the BAX gene, and it functions by forming pores in the outer membrane of the mitochondria, leading to the release of cytochrome c and other pro-apoptotic factors into the cytosol. This triggers a cascade of events that ultimately leads to cell death.

Dysregulation of BAX and other BCL-2 family proteins has been implicated in various diseases, including cancer and neurodegenerative disorders. For example, reduced levels of BAX have been observed in some types of cancer, which may contribute to tumor growth and resistance to chemotherapy. On the other hand, excessive activation of BAX has been linked to neuronal death in conditions such as Alzheimer's disease and Parkinson's disease.

A precancerous condition, also known as a premalignant condition, is a state of abnormal cellular growth and development that has a higher-than-normal potential to progress into cancer. These conditions are characterized by the presence of certain anomalies in the cells, such as dysplasia (abnormal changes in cell shape or size), which can indicate an increased risk for malignant transformation.

It is important to note that not all precancerous conditions will eventually develop into cancer, and some may even regress on their own. However, individuals with precancerous conditions are often at a higher risk of developing cancer compared to the general population. Regular monitoring and appropriate medical interventions, if necessary, can help manage this risk and potentially prevent or detect cancer at an early stage when it is more treatable.

Examples of precancerous conditions include:

1. Dysplasia in the cervix (cervical intraepithelial neoplasia or CIN)
2. Atypical ductal hyperplasia or lobular hyperplasia in the breast
3. Actinic keratosis on the skin
4. Leukoplakia in the mouth
5. Barrett's esophagus in the digestive tract

Regular medical check-ups, screenings, and lifestyle modifications are crucial for individuals with precancerous conditions to monitor their health and reduce the risk of cancer development.

'Gene expression regulation' refers to the processes that control whether, when, and where a particular gene is expressed, meaning the production of a specific protein or functional RNA encoded by that gene. This complex mechanism can be influenced by various factors such as transcription factors, chromatin remodeling, DNA methylation, non-coding RNAs, and post-transcriptional modifications, among others. Proper regulation of gene expression is crucial for normal cellular function, development, and maintaining homeostasis in living organisms. Dysregulation of gene expression can lead to various diseases, including cancer and genetic disorders.

Gene silencing is a process by which the expression of a gene is blocked or inhibited, preventing the production of its corresponding protein. This can occur naturally through various mechanisms such as RNA interference (RNAi), where small RNAs bind to and degrade specific mRNAs, or DNA methylation, where methyl groups are added to the DNA molecule, preventing transcription. Gene silencing can also be induced artificially using techniques such as RNAi-based therapies, antisense oligonucleotides, or CRISPR-Cas9 systems, which allow for targeted suppression of gene expression in research and therapeutic applications.

A point mutation is a type of genetic mutation where a single nucleotide base (A, T, C, or G) in DNA is altered, deleted, or substituted with another nucleotide. Point mutations can have various effects on the organism, depending on the location of the mutation and whether it affects the function of any genes. Some point mutations may not have any noticeable effect, while others might lead to changes in the amino acids that make up proteins, potentially causing diseases or altering traits. Point mutations can occur spontaneously due to errors during DNA replication or be inherited from parents.

Adenoviridae is a family of viruses that includes many species that can cause various types of illnesses in humans and animals. These viruses are non-enveloped, meaning they do not have a lipid membrane, and have an icosahedral symmetry with a diameter of approximately 70-90 nanometers.

The genome of Adenoviridae is composed of double-stranded DNA, which contains linear chromosomes ranging from 26 to 45 kilobases in length. The family is divided into five genera: Mastadenovirus, Aviadenovirus, Atadenovirus, Siadenovirus, and Ichtadenovirus.

Human adenoviruses are classified under the genus Mastadenovirus and can cause a wide range of illnesses, including respiratory infections, conjunctivitis, gastroenteritis, and upper respiratory tract infections. Some serotypes have also been associated with more severe diseases such as hemorrhagic cystitis, hepatitis, and meningoencephalitis.

Adenoviruses are highly contagious and can be transmitted through respiratory droplets, fecal-oral route, or by contact with contaminated surfaces. They can also be spread through contaminated water sources. Infections caused by adenoviruses are usually self-limiting, but severe cases may require hospitalization and supportive care.

Genetic transcription is the process by which the information in a strand of DNA is used to create a complementary RNA molecule. This process is the first step in gene expression, where the genetic code in DNA is converted into a form that can be used to produce proteins or functional RNAs.

During transcription, an enzyme called RNA polymerase binds to the DNA template strand and reads the sequence of nucleotide bases. As it moves along the template, it adds complementary RNA nucleotides to the growing RNA chain, creating a single-stranded RNA molecule that is complementary to the DNA template strand. Once transcription is complete, the RNA molecule may undergo further processing before it can be translated into protein or perform its functional role in the cell.

Transcription can be either "constitutive" or "regulated." Constitutive transcription occurs at a relatively constant rate and produces essential proteins that are required for basic cellular functions. Regulated transcription, on the other hand, is subject to control by various intracellular and extracellular signals, allowing cells to respond to changing environmental conditions or developmental cues.

CpG islands are defined as short stretches of DNA that are characterized by a higher than expected frequency of CpG dinucleotides. A dinucleotide is a pair of adjacent nucleotides, and in the case of CpG, C represents cytosine and G represents guanine. These islands are typically found in the promoter regions of genes, where they play important roles in regulating gene expression.

Under normal circumstances, the cytosine residue in a CpG dinucleotide is often methylated, meaning that a methyl group (-CH3) is added to the cytosine base. However, in CpG islands, methylation is usually avoided, and these regions tend to be unmethylated. This has important implications for gene expression because methylation of CpG dinucleotides in promoter regions can lead to the silencing of genes.

CpG islands are also often targets for transcription factors, which bind to specific DNA sequences and help regulate gene expression. The unmethylated state of CpG islands is thought to be important for maintaining the accessibility of these regions to transcription factors and other regulatory proteins.

Abnormal methylation patterns in CpG islands have been associated with various diseases, including cancer. In many cancers, CpG islands become aberrantly methylated, leading to the silencing of tumor suppressor genes and contributing to the development and progression of the disease.

DNA primers are short single-stranded DNA molecules that serve as a starting point for DNA synthesis. They are typically used in laboratory techniques such as the polymerase chain reaction (PCR) and DNA sequencing. The primer binds to a complementary sequence on the DNA template through base pairing, providing a free 3'-hydroxyl group for the DNA polymerase enzyme to add nucleotides and synthesize a new strand of DNA. This allows for specific and targeted amplification or analysis of a particular region of interest within a larger DNA molecule.

The term "DNA, neoplasm" is not a standard medical term or concept. DNA refers to deoxyribonucleic acid, which is the genetic material present in the cells of living organisms. A neoplasm, on the other hand, is a tumor or growth of abnormal tissue that can be benign (non-cancerous) or malignant (cancerous).

In some contexts, "DNA, neoplasm" may refer to genetic alterations found in cancer cells. These genetic changes can include mutations, amplifications, deletions, or rearrangements of DNA sequences that contribute to the development and progression of cancer. Identifying these genetic abnormalities can help doctors diagnose and treat certain types of cancer more effectively.

However, it's important to note that "DNA, neoplasm" is not a term that would typically be used in medical reports or research papers without further clarification. If you have any specific questions about DNA changes in cancer cells or neoplasms, I would recommend consulting with a healthcare professional or conducting further research on the topic.

A neoplasm is a tumor or growth that is formed by an abnormal and excessive proliferation of cells, which can be benign or malignant. Neoplasm proteins are therefore any proteins that are expressed or produced in these neoplastic cells. These proteins can play various roles in the development, progression, and maintenance of neoplasms.

Some neoplasm proteins may contribute to the uncontrolled cell growth and division seen in cancer, such as oncogenic proteins that promote cell cycle progression or inhibit apoptosis (programmed cell death). Others may help the neoplastic cells evade the immune system, allowing them to proliferate undetected. Still others may be involved in angiogenesis, the formation of new blood vessels that supply the tumor with nutrients and oxygen.

Neoplasm proteins can also serve as biomarkers for cancer diagnosis, prognosis, or treatment response. For example, the presence or level of certain neoplasm proteins in biological samples such as blood or tissue may indicate the presence of a specific type of cancer, help predict the likelihood of cancer recurrence, or suggest whether a particular therapy will be effective.

Overall, understanding the roles and behaviors of neoplasm proteins can provide valuable insights into the biology of cancer and inform the development of new diagnostic and therapeutic strategies.

DNA Mutational Analysis is a laboratory test used to identify genetic variations or changes (mutations) in the DNA sequence of a gene. This type of analysis can be used to diagnose genetic disorders, predict the risk of developing certain diseases, determine the most effective treatment for cancer, or assess the likelihood of passing on an inherited condition to offspring.

The test involves extracting DNA from a patient's sample (such as blood, saliva, or tissue), amplifying specific regions of interest using polymerase chain reaction (PCR), and then sequencing those regions to determine the precise order of nucleotide bases in the DNA molecule. The resulting sequence is then compared to reference sequences to identify any variations or mutations that may be present.

DNA Mutational Analysis can detect a wide range of genetic changes, including single-nucleotide polymorphisms (SNPs), insertions, deletions, duplications, and rearrangements. The test is often used in conjunction with other diagnostic tests and clinical evaluations to provide a comprehensive assessment of a patient's genetic profile.

It is important to note that not all mutations are pathogenic or associated with disease, and the interpretation of DNA Mutational Analysis results requires careful consideration of the patient's medical history, family history, and other relevant factors.

Apoptosis regulatory proteins are a group of proteins that play an essential role in the regulation and execution of apoptosis, also known as programmed cell death. This process is a normal part of development and tissue homeostasis, allowing for the elimination of damaged or unnecessary cells. The balance between pro-apoptotic and anti-apoptotic proteins determines whether a cell will undergo apoptosis.

Pro-apoptotic proteins, such as BAX, BID, and PUMA, promote apoptosis by neutralizing or counteracting the effects of anti-apoptotic proteins or by directly activating the apoptotic pathway. These proteins can be activated in response to various stimuli, including DNA damage, oxidative stress, and activation of the death receptor pathway.

Anti-apoptotic proteins, such as BCL-2, BCL-XL, and MCL-1, inhibit apoptosis by binding and neutralizing pro-apoptotic proteins or by preventing the release of cytochrome c from the mitochondria, which is a key step in the intrinsic apoptotic pathway.

Dysregulation of apoptosis regulatory proteins has been implicated in various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. Therefore, understanding the role of these proteins in apoptosis regulation is crucial for developing new therapeutic strategies to treat these conditions.

Carcinogens are agents (substances or mixtures of substances) that can cause cancer. They may be naturally occurring or man-made. Carcinogens can increase the risk of cancer by altering cellular DNA, disrupting cellular function, or promoting cell growth. Examples of carcinogens include certain chemicals found in tobacco smoke, asbestos, UV radiation from the sun, and some viruses.

It's important to note that not all exposures to carcinogens will result in cancer, and the risk typically depends on factors such as the level and duration of exposure, individual genetic susceptibility, and lifestyle choices. The International Agency for Research on Cancer (IARC) classifies carcinogens into different groups based on the strength of evidence linking them to cancer:

Group 1: Carcinogenic to humans
Group 2A: Probably carcinogenic to humans
Group 2B: Possibly carcinogenic to humans
Group 3: Not classifiable as to its carcinogenicity to humans
Group 4: Probably not carcinogenic to humans

This information is based on medical research and may be subject to change as new studies become available. Always consult a healthcare professional for medical advice.

Western blotting is a laboratory technique used in molecular biology to detect and quantify specific proteins in a mixture of many different proteins. This technique is commonly used to confirm the expression of a protein of interest, determine its size, and investigate its post-translational modifications. The name "Western" blotting distinguishes this technique from Southern blotting (for DNA) and Northern blotting (for RNA).

The Western blotting procedure involves several steps:

1. Protein extraction: The sample containing the proteins of interest is first extracted, often by breaking open cells or tissues and using a buffer to extract the proteins.
2. Separation of proteins by electrophoresis: The extracted proteins are then separated based on their size by loading them onto a polyacrylamide gel and running an electric current through the gel (a process called sodium dodecyl sulfate-polyacrylamide gel electrophoresis or SDS-PAGE). This separates the proteins according to their molecular weight, with smaller proteins migrating faster than larger ones.
3. Transfer of proteins to a membrane: After separation, the proteins are transferred from the gel onto a nitrocellulose or polyvinylidene fluoride (PVDF) membrane using an electric current in a process called blotting. This creates a replica of the protein pattern on the gel but now immobilized on the membrane for further analysis.
4. Blocking: The membrane is then blocked with a blocking agent, such as non-fat dry milk or bovine serum albumin (BSA), to prevent non-specific binding of antibodies in subsequent steps.
5. Primary antibody incubation: A primary antibody that specifically recognizes the protein of interest is added and allowed to bind to its target protein on the membrane. This step may be performed at room temperature or 4°C overnight, depending on the antibody's properties.
6. Washing: The membrane is washed with a buffer to remove unbound primary antibodies.
7. Secondary antibody incubation: A secondary antibody that recognizes the primary antibody (often coupled to an enzyme or fluorophore) is added and allowed to bind to the primary antibody. This step may involve using a horseradish peroxidase (HRP)-conjugated or alkaline phosphatase (AP)-conjugated secondary antibody, depending on the detection method used later.
8. Washing: The membrane is washed again to remove unbound secondary antibodies.
9. Detection: A detection reagent is added to visualize the protein of interest by detecting the signal generated from the enzyme-conjugated or fluorophore-conjugated secondary antibody. This can be done using chemiluminescent, colorimetric, or fluorescent methods.
10. Analysis: The resulting image is analyzed to determine the presence and quantity of the protein of interest in the sample.

Western blotting is a powerful technique for identifying and quantifying specific proteins within complex mixtures. It can be used to study protein expression, post-translational modifications, protein-protein interactions, and more. However, it requires careful optimization and validation to ensure accurate and reproducible results.

Viral genes refer to the genetic material present in viruses that contains the information necessary for their replication and the production of viral proteins. In DNA viruses, the genetic material is composed of double-stranded or single-stranded DNA, while in RNA viruses, it is composed of single-stranded or double-stranded RNA.

Viral genes can be classified into three categories: early, late, and structural. Early genes encode proteins involved in the replication of the viral genome, modulation of host cell processes, and regulation of viral gene expression. Late genes encode structural proteins that make up the viral capsid or envelope. Some viruses also have structural genes that are expressed throughout their replication cycle.

Understanding the genetic makeup of viruses is crucial for developing antiviral therapies and vaccines. By targeting specific viral genes, researchers can develop drugs that inhibit viral replication and reduce the severity of viral infections. Additionally, knowledge of viral gene sequences can inform the development of vaccines that stimulate an immune response to specific viral proteins.

Neoplastic cell transformation is a process in which a normal cell undergoes genetic alterations that cause it to become cancerous or malignant. This process involves changes in the cell's DNA that result in uncontrolled cell growth and division, loss of contact inhibition, and the ability to invade surrounding tissues and metastasize (spread) to other parts of the body.

Neoplastic transformation can occur as a result of various factors, including genetic mutations, exposure to carcinogens, viral infections, chronic inflammation, and aging. These changes can lead to the activation of oncogenes or the inactivation of tumor suppressor genes, which regulate cell growth and division.

The transformation of normal cells into cancerous cells is a complex and multi-step process that involves multiple genetic and epigenetic alterations. It is characterized by several hallmarks, including sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, enabling replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evading immune destruction.

Neoplastic cell transformation is a fundamental concept in cancer biology and is critical for understanding the molecular mechanisms underlying cancer development and progression. It also has important implications for cancer diagnosis, prognosis, and treatment, as identifying the specific genetic alterations that underlie neoplastic transformation can help guide targeted therapies and personalized medicine approaches.

Cyclin-dependent kinases (CDKs) are a family of serine/threonine protein kinases that play crucial roles in regulating the cell cycle, transcription, and other cellular processes. They are activated by binding to cyclin proteins, which accumulate and degrade at specific stages of the cell cycle. The activation of CDKs leads to phosphorylation of various downstream target proteins, resulting in the promotion or inhibition of different cell cycle events. Dysregulation of CDKs has been implicated in several human diseases, including cancer, and they are considered important targets for drug development.

An allele is a variant form of a gene that is located at a specific position on a specific chromosome. Alleles are alternative forms of the same gene that arise by mutation and are found at the same locus or position on homologous chromosomes.

Each person typically inherits two copies of each gene, one from each parent. If the two alleles are identical, a person is said to be homozygous for that trait. If the alleles are different, the person is heterozygous.

For example, the ABO blood group system has three alleles, A, B, and O, which determine a person's blood type. If a person inherits two A alleles, they will have type A blood; if they inherit one A and one B allele, they will have type AB blood; if they inherit two B alleles, they will have type B blood; and if they inherit two O alleles, they will have type O blood.

Alleles can also influence traits such as eye color, hair color, height, and other physical characteristics. Some alleles are dominant, meaning that only one copy of the allele is needed to express the trait, while others are recessive, meaning that two copies of the allele are needed to express the trait.

Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) is a laboratory technique used in molecular biology to amplify and detect specific DNA sequences. This technique is particularly useful for the detection and quantification of RNA viruses, as well as for the analysis of gene expression.

The process involves two main steps: reverse transcription and polymerase chain reaction (PCR). In the first step, reverse transcriptase enzyme is used to convert RNA into complementary DNA (cDNA) by reading the template provided by the RNA molecule. This cDNA then serves as a template for the PCR amplification step.

In the second step, the PCR reaction uses two primers that flank the target DNA sequence and a thermostable polymerase enzyme to repeatedly copy the targeted cDNA sequence. The reaction mixture is heated and cooled in cycles, allowing the primers to anneal to the template, and the polymerase to extend the new strand. This results in exponential amplification of the target DNA sequence, making it possible to detect even small amounts of RNA or cDNA.

RT-PCR is a sensitive and specific technique that has many applications in medical research and diagnostics, including the detection of viruses such as HIV, hepatitis C virus, and SARS-CoV-2 (the virus that causes COVID-19). It can also be used to study gene expression, identify genetic mutations, and diagnose genetic disorders.

Proto-oncogene proteins, such as c-Myc, are crucial regulators of normal cell growth, differentiation, and apoptosis (programmed cell death). When proto-oncogenes undergo mutations or alterations in their regulation, they can become overactive or overexpressed, leading to the formation of oncogenes. Oncogenic forms of c-Myc contribute to uncontrolled cell growth and division, which can ultimately result in cancer development.

The c-Myc protein is a transcription factor that binds to specific DNA sequences, influencing the expression of target genes involved in various cellular processes, such as:

1. Cell cycle progression: c-Myc promotes the expression of genes required for the G1 to S phase transition, driving cells into the DNA synthesis and division phase.
2. Metabolism: c-Myc regulates genes associated with glucose metabolism, glycolysis, and mitochondrial function, enhancing energy production in rapidly dividing cells.
3. Apoptosis: c-Myc can either promote or inhibit apoptosis, depending on the cellular context and the presence of other regulatory factors.
4. Differentiation: c-Myc generally inhibits differentiation by repressing genes that are necessary for specialized cell functions.
5. Angiogenesis: c-Myc can induce the expression of pro-angiogenic factors, promoting the formation of new blood vessels to support tumor growth.

Dysregulation of c-Myc is frequently observed in various types of cancer, making it an important therapeutic target for cancer treatment.

Adenocarcinoma is a type of cancer that arises from glandular epithelial cells. These cells line the inside of many internal organs, including the breasts, prostate, colon, and lungs. Adenocarcinomas can occur in any of these organs, as well as in other locations where glands are present.

The term "adenocarcinoma" is used to describe a cancer that has features of glandular tissue, such as mucus-secreting cells or cells that produce hormones. These cancers often form glandular structures within the tumor mass and may produce mucus or other substances.

Adenocarcinomas are typically slow-growing and tend to spread (metastasize) to other parts of the body through the lymphatic system or bloodstream. They can be treated with surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these treatments. The prognosis for adenocarcinoma depends on several factors, including the location and stage of the cancer, as well as the patient's overall health and age.

Skin neoplasms refer to abnormal growths or tumors in the skin that can be benign (non-cancerous) or malignant (cancerous). They result from uncontrolled multiplication of skin cells, which can form various types of lesions. These growths may appear as lumps, bumps, sores, patches, or discolored areas on the skin.

Benign skin neoplasms include conditions such as moles, warts, and seborrheic keratoses, while malignant skin neoplasms are primarily classified into melanoma, squamous cell carcinoma, and basal cell carcinoma. These three types of cancerous skin growths are collectively known as non-melanoma skin cancers (NMSCs). Melanoma is the most aggressive and dangerous form of skin cancer, while NMSCs tend to be less invasive but more common.

It's essential to monitor any changes in existing skin lesions or the appearance of new growths and consult a healthcare professional for proper evaluation and treatment if needed.

Squamous cell carcinoma is a type of skin cancer that begins in the squamous cells, which are flat, thin cells that form the outer layer of the skin (epidermis). It commonly occurs on sun-exposed areas such as the face, ears, lips, and backs of the hands. Squamous cell carcinoma can also develop in other areas of the body including the mouth, lungs, and cervix.

This type of cancer usually develops slowly and may appear as a rough or scaly patch of skin, a red, firm nodule, or a sore or ulcer that doesn't heal. While squamous cell carcinoma is not as aggressive as some other types of cancer, it can metastasize (spread) to other parts of the body if left untreated, making early detection and treatment important.

Risk factors for developing squamous cell carcinoma include prolonged exposure to ultraviolet (UV) radiation from the sun or tanning beds, fair skin, a history of sunburns, a weakened immune system, and older age. Prevention measures include protecting your skin from the sun by wearing protective clothing, using a broad-spectrum sunscreen with an SPF of at least 30, avoiding tanning beds, and getting regular skin examinations.

A genetic vector is a vehicle, often a plasmid or a virus, that is used to introduce foreign DNA into a host cell as part of genetic engineering or gene therapy techniques. The vector contains the desired gene or genes, along with regulatory elements such as promoters and enhancers, which are needed for the expression of the gene in the target cells.

The choice of vector depends on several factors, including the size of the DNA to be inserted, the type of cell to be targeted, and the efficiency of uptake and expression required. Commonly used vectors include plasmids, adenoviruses, retroviruses, and lentiviruses.

Plasmids are small circular DNA molecules that can replicate independently in bacteria. They are often used as cloning vectors to amplify and manipulate DNA fragments. Adenoviruses are double-stranded DNA viruses that infect a wide range of host cells, including human cells. They are commonly used as gene therapy vectors because they can efficiently transfer genes into both dividing and non-dividing cells.

Retroviruses and lentiviruses are RNA viruses that integrate their genetic material into the host cell's genome. This allows for stable expression of the transgene over time. Lentiviruses, a subclass of retroviruses, have the advantage of being able to infect non-dividing cells, making them useful for gene therapy applications in post-mitotic tissues such as neurons and muscle cells.

Overall, genetic vectors play a crucial role in modern molecular biology and medicine, enabling researchers to study gene function, develop new therapies, and modify organisms for various purposes.

Repressor proteins are a type of regulatory protein in molecular biology that suppress the transcription of specific genes into messenger RNA (mRNA) by binding to DNA. They function as part of gene regulation processes, often working in conjunction with an operator region and a promoter region within the DNA molecule. Repressor proteins can be activated or deactivated by various signals, allowing for precise control over gene expression in response to changing cellular conditions.

There are two main types of repressor proteins:

1. DNA-binding repressors: These directly bind to specific DNA sequences (operator regions) near the target gene and prevent RNA polymerase from transcribing the gene into mRNA.
2. Allosteric repressors: These bind to effector molecules, which then cause a conformational change in the repressor protein, enabling it to bind to DNA and inhibit transcription.

Repressor proteins play crucial roles in various biological processes, such as development, metabolism, and stress response, by controlling gene expression patterns in cells.

Acetylation is a chemical process that involves the addition of an acetyl group (-COCH3) to a molecule. In the context of medical biochemistry, acetylation often refers to the post-translational modification of proteins, where an acetyl group is added to the amino group of a lysine residue in a protein by an enzyme called acetyltransferase. This modification can alter the function or stability of the protein and plays a crucial role in regulating various cellular processes such as gene expression, DNA repair, and cell signaling. Acetylation can also occur on other types of molecules, including lipids and carbohydrates, and has important implications for drug metabolism and toxicity.

Retinoblastoma Protein (pRb or RB1) is a tumor suppressor protein that plays a critical role in regulating the cell cycle and preventing uncontrolled cell growth. It is encoded by the RB1 gene, located on chromosome 13. The retinoblastoma protein functions as a regulatory checkpoint in the cell cycle, preventing cells from progressing into the S phase (DNA synthesis phase) until certain conditions are met.

When pRb is in its active state, it binds to and inhibits the activity of E2F transcription factors, which promote the expression of genes required for DNA replication and cell cycle progression. Phosphorylation of pRb by cyclin-dependent kinases (CDKs) leads to the release of E2F factors, allowing them to activate their target genes and drive the cell into S phase.

Mutations in the RB1 gene can result in the production of a nonfunctional or reduced amount of pRb protein, leading to uncontrolled cell growth and an increased risk of developing retinoblastoma, a rare form of eye cancer, as well as other types of tumors.

Cell proliferation is the process by which cells increase in number, typically through the process of cell division. In the context of biology and medicine, it refers to the reproduction of cells that makes up living tissue, allowing growth, maintenance, and repair. It involves several stages including the transition from a phase of quiescence (G0 phase) to an active phase (G1 phase), DNA replication in the S phase, and mitosis or M phase, where the cell divides into two daughter cells.

Abnormal or uncontrolled cell proliferation is a characteristic feature of many diseases, including cancer, where deregulated cell cycle control leads to excessive and unregulated growth of cells, forming tumors that can invade surrounding tissues and metastasize to distant sites in the body.

Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.

Ras genes are a group of genes that encode for proteins involved in cell signaling pathways that regulate cell growth, differentiation, and survival. Mutations in Ras genes have been associated with various types of cancer, as well as other diseases such as developmental disorders and autoimmune diseases. The Ras protein family includes H-Ras, K-Ras, and N-Ras, which are activated by growth factor receptors and other signals to activate downstream effectors involved in cell proliferation and survival. Abnormal activation of Ras signaling due to mutations or dysregulation can contribute to tumor development and progression.

"Nude mice" is a term used in the field of laboratory research to describe a strain of mice that have been genetically engineered to lack a functional immune system. Specifically, nude mice lack a thymus gland and have a mutation in the FOXN1 gene, which results in a failure to develop a mature T-cell population. This means that they are unable to mount an effective immune response against foreign substances or organisms.

The name "nude" refers to the fact that these mice also have a lack of functional hair follicles, resulting in a hairless or partially hairless phenotype. This feature is actually a secondary consequence of the same genetic mutation that causes their immune deficiency.

Nude mice are commonly used in research because their weakened immune system makes them an ideal host for transplanted tumors, tissues, and cells from other species, including humans. This allows researchers to study the behavior of these foreign substances in a living organism without the complication of an immune response. However, it's important to note that because nude mice lack a functional immune system, they must be kept in sterile conditions and are more susceptible to infection than normal mice.

Down-regulation is a process that occurs in response to various stimuli, where the number or sensitivity of cell surface receptors or the expression of specific genes is decreased. This process helps maintain homeostasis within cells and tissues by reducing the ability of cells to respond to certain signals or molecules.

In the context of cell surface receptors, down-regulation can occur through several mechanisms:

1. Receptor internalization: After binding to their ligands, receptors can be internalized into the cell through endocytosis. Once inside the cell, these receptors may be degraded or recycled back to the cell surface in smaller numbers.
2. Reduced receptor synthesis: Down-regulation can also occur at the transcriptional level, where the expression of genes encoding for specific receptors is decreased, leading to fewer receptors being produced.
3. Receptor desensitization: Prolonged exposure to a ligand can lead to a decrease in receptor sensitivity or affinity, making it more difficult for the cell to respond to the signal.

In the context of gene expression, down-regulation refers to the decreased transcription and/or stability of specific mRNAs, leading to reduced protein levels. This process can be induced by various factors, including microRNA (miRNA)-mediated regulation, histone modification, or DNA methylation.

Down-regulation is an essential mechanism in many physiological processes and can also contribute to the development of several diseases, such as cancer and neurodegenerative disorders.

The cell nucleus is a membrane-bound organelle found in the eukaryotic cells (cells with a true nucleus). It contains most of the cell's genetic material, organized as DNA molecules in complex with proteins, RNA molecules, and histones to form chromosomes.

The primary function of the cell nucleus is to regulate and control the activities of the cell, including growth, metabolism, protein synthesis, and reproduction. It also plays a crucial role in the process of mitosis (cell division) by separating and protecting the genetic material during this process. The nuclear membrane, or nuclear envelope, surrounding the nucleus is composed of two lipid bilayers with numerous pores that allow for the selective transport of molecules between the nucleoplasm (nucleus interior) and the cytoplasm (cell exterior).

The cell nucleus is a vital structure in eukaryotic cells, and its dysfunction can lead to various diseases, including cancer and genetic disorders.

Fibroblasts are specialized cells that play a critical role in the body's immune response and wound healing process. They are responsible for producing and maintaining the extracellular matrix (ECM), which is the non-cellular component present within all tissues and organs, providing structural support and biochemical signals for surrounding cells.

Fibroblasts produce various ECM proteins such as collagens, elastin, fibronectin, and laminins, forming a complex network of fibers that give tissues their strength and flexibility. They also help in the regulation of tissue homeostasis by controlling the turnover of ECM components through the process of remodeling.

In response to injury or infection, fibroblasts become activated and start to proliferate rapidly, migrating towards the site of damage. Here, they participate in the inflammatory response, releasing cytokines and chemokines that attract immune cells to the area. Additionally, they deposit new ECM components to help repair the damaged tissue and restore its functionality.

Dysregulation of fibroblast activity has been implicated in several pathological conditions, including fibrosis (excessive scarring), cancer (where they can contribute to tumor growth and progression), and autoimmune diseases (such as rheumatoid arthritis).

Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.

The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.

Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.

Flow cytometry is a medical and research technique used to measure physical and chemical characteristics of cells or particles, one cell at a time, as they flow in a fluid stream through a beam of light. The properties measured include:

* Cell size (light scatter)
* Cell internal complexity (granularity, also light scatter)
* Presence or absence of specific proteins or other molecules on the cell surface or inside the cell (using fluorescent antibodies or other fluorescent probes)

The technique is widely used in cell counting, cell sorting, protein engineering, biomarker discovery and monitoring disease progression, particularly in hematology, immunology, and cancer research.

Lung neoplasms refer to abnormal growths or tumors in the lung tissue. These tumors can be benign (non-cancerous) or malignant (cancerous). Malignant lung neoplasms are further classified into two main types: small cell lung carcinoma and non-small cell lung carcinoma. Lung neoplasms can cause symptoms such as cough, chest pain, shortness of breath, and weight loss. They are often caused by smoking or exposure to secondhand smoke, but can also occur due to genetic factors, radiation exposure, and other environmental carcinogens. Early detection and treatment of lung neoplasms is crucial for improving outcomes and survival rates.

Neoplasms are abnormal growths of cells or tissues in the body that serve no physiological function. They can be benign (non-cancerous) or malignant (cancerous). Benign neoplasms are typically slow growing and do not spread to other parts of the body, while malignant neoplasms are aggressive, invasive, and can metastasize to distant sites.

Neoplasms occur when there is a dysregulation in the normal process of cell division and differentiation, leading to uncontrolled growth and accumulation of cells. This can result from genetic mutations or other factors such as viral infections, environmental exposures, or hormonal imbalances.

Neoplasms can develop in any organ or tissue of the body and can cause various symptoms depending on their size, location, and type. Treatment options for neoplasms include surgery, radiation therapy, chemotherapy, immunotherapy, and targeted therapy, among others.

Viral proteins are the proteins that are encoded by the viral genome and are essential for the viral life cycle. These proteins can be structural or non-structural and play various roles in the virus's replication, infection, and assembly process. Structural proteins make up the physical structure of the virus, including the capsid (the protein shell that surrounds the viral genome) and any envelope proteins (that may be present on enveloped viruses). Non-structural proteins are involved in the replication of the viral genome and modulation of the host cell environment to favor viral replication. Overall, a thorough understanding of viral proteins is crucial for developing antiviral therapies and vaccines.

Trans-activators are proteins that increase the transcriptional activity of a gene or a set of genes. They do this by binding to specific DNA sequences and interacting with the transcription machinery, thereby enhancing the recruitment and assembly of the complexes needed for transcription. In some cases, trans-activators can also modulate the chromatin structure to make the template more accessible to the transcription machinery.

In the context of HIV (Human Immunodeficiency Virus) infection, the term "trans-activator" is often used specifically to refer to the Tat protein. The Tat protein is a viral regulatory protein that plays a critical role in the replication of HIV by activating the transcription of the viral genome. It does this by binding to a specific RNA structure called the Trans-Activation Response Element (TAR) located at the 5' end of all nascent HIV transcripts, and recruiting cellular cofactors that enhance the processivity and efficiency of RNA polymerase II, leading to increased viral gene expression.

Tumor markers are substances that can be found in the body and their presence can indicate the presence of certain types of cancer or other conditions. Biological tumor markers refer to those substances that are produced by cancer cells or by other cells in response to cancer or certain benign (non-cancerous) conditions. These markers can be found in various bodily fluids such as blood, urine, or tissue samples.

Examples of biological tumor markers include:

1. Proteins: Some tumor markers are proteins that are produced by cancer cells or by other cells in response to the presence of cancer. For example, prostate-specific antigen (PSA) is a protein produced by normal prostate cells and in higher amounts by prostate cancer cells.
2. Genetic material: Tumor markers can also include genetic material such as DNA, RNA, or microRNA that are shed by cancer cells into bodily fluids. For example, circulating tumor DNA (ctDNA) is genetic material from cancer cells that can be found in the bloodstream.
3. Metabolites: Tumor markers can also include metabolic products produced by cancer cells or by other cells in response to cancer. For example, lactate dehydrogenase (LDH) is an enzyme that is released into the bloodstream when cancer cells break down glucose for energy.

It's important to note that tumor markers are not specific to cancer and can be elevated in non-cancerous conditions as well. Therefore, they should not be used alone to diagnose cancer but rather as a tool in conjunction with other diagnostic tests and clinical evaluations.

Phosphorylation is the process of adding a phosphate group (a molecule consisting of one phosphorus atom and four oxygen atoms) to a protein or other organic molecule, which is usually done by enzymes called kinases. This post-translational modification can change the function, localization, or activity of the target molecule, playing a crucial role in various cellular processes such as signal transduction, metabolism, and regulation of gene expression. Phosphorylation is reversible, and the removal of the phosphate group is facilitated by enzymes called phosphatases.

DNA Sequence Analysis is the systematic determination of the order of nucleotides in a DNA molecule. It is a critical component of modern molecular biology, genetics, and genetic engineering. The process involves determining the exact order of the four nucleotide bases - adenine (A), guanine (G), cytosine (C), and thymine (T) - in a DNA molecule or fragment. This information is used in various applications such as identifying gene mutations, studying evolutionary relationships, developing molecular markers for breeding, and diagnosing genetic diseases.

The process of DNA Sequence Analysis typically involves several steps, including DNA extraction, PCR amplification (if necessary), purification, sequencing reaction, and electrophoresis. The resulting data is then analyzed using specialized software to determine the exact sequence of nucleotides.

In recent years, high-throughput DNA sequencing technologies have revolutionized the field of genomics, enabling the rapid and cost-effective sequencing of entire genomes. This has led to an explosion of genomic data and new insights into the genetic basis of many diseases and traits.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Up-regulation is a term used in molecular biology and medicine to describe an increase in the expression or activity of a gene, protein, or receptor in response to a stimulus. This can occur through various mechanisms such as increased transcription, translation, or reduced degradation of the molecule. Up-regulation can have important functional consequences, for example, enhancing the sensitivity or response of a cell to a hormone, neurotransmitter, or drug. It is a normal physiological process that can also be induced by disease or pharmacological interventions.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

Genetic polymorphism refers to the occurrence of multiple forms (called alleles) of a particular gene within a population. These variations in the DNA sequence do not generally affect the function or survival of the organism, but they can contribute to differences in traits among individuals. Genetic polymorphisms can be caused by single nucleotide changes (SNPs), insertions or deletions of DNA segments, or other types of genetic rearrangements. They are important for understanding genetic diversity and evolution, as well as for identifying genetic factors that may contribute to disease susceptibility in humans.

Deoxyribonucleic acid (DNA) is the genetic material present in the cells of organisms where it is responsible for the storage and transmission of hereditary information. DNA is a long molecule that consists of two strands coiled together to form a double helix. Each strand is made up of a series of four nucleotide bases - adenine (A), guanine (G), cytosine (C), and thymine (T) - that are linked together by phosphate and sugar groups. The sequence of these bases along the length of the molecule encodes genetic information, with A always pairing with T and C always pairing with G. This base-pairing allows for the replication and transcription of DNA, which are essential processes in the functioning and reproduction of all living organisms.

A plasmid is a small, circular, double-stranded DNA molecule that is separate from the chromosomal DNA of a bacterium or other organism. Plasmids are typically not essential for the survival of the organism, but they can confer beneficial traits such as antibiotic resistance or the ability to degrade certain types of pollutants.

Plasmids are capable of replicating independently of the chromosomal DNA and can be transferred between bacteria through a process called conjugation. They often contain genes that provide resistance to antibiotics, heavy metals, and other environmental stressors. Plasmids have also been engineered for use in molecular biology as cloning vectors, allowing scientists to replicate and manipulate specific DNA sequences.

Plasmids are important tools in genetic engineering and biotechnology because they can be easily manipulated and transferred between organisms. They have been used to produce vaccines, diagnostic tests, and genetically modified organisms (GMOs) for various applications, including agriculture, medicine, and industry.

Epithelial cells are types of cells that cover the outer surfaces of the body, line the inner surfaces of organs and glands, and form the lining of blood vessels and body cavities. They provide a protective barrier against the external environment, regulate the movement of materials between the internal and external environments, and are involved in the sense of touch, temperature, and pain. Epithelial cells can be squamous (flat and thin), cuboidal (square-shaped and of equal height), or columnar (tall and narrow) in shape and are classified based on their location and function.

Breast neoplasms refer to abnormal growths in the breast tissue that can be benign or malignant. Benign breast neoplasms are non-cancerous tumors or growths, while malignant breast neoplasms are cancerous tumors that can invade surrounding tissues and spread to other parts of the body.

Breast neoplasms can arise from different types of cells in the breast, including milk ducts, milk sacs (lobules), or connective tissue. The most common type of breast cancer is ductal carcinoma, which starts in the milk ducts and can spread to other parts of the breast and nearby structures.

Breast neoplasms are usually detected through screening methods such as mammography, ultrasound, or MRI, or through self-examination or clinical examination. Treatment options for breast neoplasms depend on several factors, including the type and stage of the tumor, the patient's age and overall health, and personal preferences. Treatment may include surgery, radiation therapy, chemotherapy, hormone therapy, or targeted therapy.

Carrier proteins, also known as transport proteins, are a type of protein that facilitates the movement of molecules across cell membranes. They are responsible for the selective and active transport of ions, sugars, amino acids, and other molecules from one side of the membrane to the other, against their concentration gradient. This process requires energy, usually in the form of ATP (adenosine triphosphate).

Carrier proteins have a specific binding site for the molecule they transport, and undergo conformational changes upon binding, which allows them to move the molecule across the membrane. Once the molecule has been transported, the carrier protein returns to its original conformation, ready to bind and transport another molecule.

Carrier proteins play a crucial role in maintaining the balance of ions and other molecules inside and outside of cells, and are essential for many physiological processes, including nerve impulse transmission, muscle contraction, and nutrient uptake.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Prognosis is a medical term that refers to the prediction of the likely outcome or course of a disease, including the chances of recovery or recurrence, based on the patient's symptoms, medical history, physical examination, and diagnostic tests. It is an important aspect of clinical decision-making and patient communication, as it helps doctors and patients make informed decisions about treatment options, set realistic expectations, and plan for future care.

Prognosis can be expressed in various ways, such as percentages, categories (e.g., good, fair, poor), or survival rates, depending on the nature of the disease and the available evidence. However, it is important to note that prognosis is not an exact science and may vary depending on individual factors, such as age, overall health status, and response to treatment. Therefore, it should be used as a guide rather than a definitive forecast.

Transgenic mice are genetically modified rodents that have incorporated foreign DNA (exogenous DNA) into their own genome. This is typically done through the use of recombinant DNA technology, where a specific gene or genetic sequence of interest is isolated and then introduced into the mouse embryo. The resulting transgenic mice can then express the protein encoded by the foreign gene, allowing researchers to study its function in a living organism.

The process of creating transgenic mice usually involves microinjecting the exogenous DNA into the pronucleus of a fertilized egg, which is then implanted into a surrogate mother. The offspring that result from this procedure are screened for the presence of the foreign DNA, and those that carry the desired genetic modification are used to establish a transgenic mouse line.

Transgenic mice have been widely used in biomedical research to model human diseases, study gene function, and test new therapies. They provide a valuable tool for understanding complex biological processes and developing new treatments for a variety of medical conditions.

Cell differentiation is the process by which a less specialized cell, or stem cell, becomes a more specialized cell type with specific functions and structures. This process involves changes in gene expression, which are regulated by various intracellular signaling pathways and transcription factors. Differentiation results in the development of distinct cell types that make up tissues and organs in multicellular organisms. It is a crucial aspect of embryonic development, tissue repair, and maintenance of homeostasis in the body.

In the context of medical and biological sciences, a "binding site" refers to a specific location on a protein, molecule, or cell where another molecule can attach or bind. This binding interaction can lead to various functional changes in the original protein or molecule. The other molecule that binds to the binding site is often referred to as a ligand, which can be a small molecule, ion, or even another protein.

The binding between a ligand and its target binding site can be specific and selective, meaning that only certain ligands can bind to particular binding sites with high affinity. This specificity plays a crucial role in various biological processes, such as signal transduction, enzyme catalysis, or drug action.

In the case of drug development, understanding the location and properties of binding sites on target proteins is essential for designing drugs that can selectively bind to these sites and modulate protein function. This knowledge can help create more effective and safer therapeutic options for various diseases.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Protein binding, in the context of medical and biological sciences, refers to the interaction between a protein and another molecule (known as the ligand) that results in a stable complex. This process is often reversible and can be influenced by various factors such as pH, temperature, and concentration of the involved molecules.

In clinical chemistry, protein binding is particularly important when it comes to drugs, as many of them bind to proteins (especially albumin) in the bloodstream. The degree of protein binding can affect a drug's distribution, metabolism, and excretion, which in turn influence its therapeutic effectiveness and potential side effects.

Protein-bound drugs may be less available for interaction with their target tissues, as only the unbound or "free" fraction of the drug is active. Therefore, understanding protein binding can help optimize dosing regimens and minimize adverse reactions.

"Entrez Gene: P53-responsive gene 1". Retrieved 2017-11-07. Ozalp S, Yalcin OT, Tanir HM, Kabukcuoglu S, Erol G (2003). "p53 ... P53-responsive gene 1 is a protein that in humans is encoded by the PRG1 gene. "Human PubMed Reference:". National Center for ... Human genes, All stub articles, Human chromosome 19 gene stubs). ... "P53 and K-ras mutations are frequent events in microscopically ...
Many cancers do exhibit p53 gene mutations, making gene therapies that target this gene[clarification needed] impossible, but ... PUMA can also function as an indicator of p53 mutations. Many cancers exhibit mutations in the p53 gene, but this mutation can ... "Activation of p53 and the pro-apoptotic p53 target gene PUMA during depolarization-induced apoptosis of chromaffin cells". Exp ... Nakano K, Vousden KH (March 2001). "PUMA, a novel proapoptotic gene, is induced by p53". Mol. Cell. 7 (3): 683-94. doi:10.1016/ ...
The p21 gene contains several p53 response elements that mediate direct binding of the p53 protein, resulting in ... Several isoforms were discovered in 2005, and so far 12 human p53 isoforms have been identified (p53α, p53β, p53γ, ∆40p53α, ∆ ... As with 95% of human genes, TP53 encodes more than one protein. All these p53 proteins are called the p53 isoforms. These ... It delivers a functional copy of the p53 gene using an engineered adenovirus. Certain pathogens can also affect the p53 protein ...
The TP53 gene (also known as p53) is crucial in ensuring the conservation of the genome. Deubiquitinating enzymes play an ... "TP53 gene". MedlinePlus. U.S. National Library of Medicine. Retrieved May 18, 2021. "p53". Wikipedia. Retrieved May 18, 2021. ... In healthy cells, p53 activates the E3 ubiquitin ligase MDM2 which in turn ubiquitinates p53. This creates a negative feedback ... Once stabilized, p53 can exert its tumor suppression function. Downstream pathways of p53 act to either halt cell cycle ...
p53. TP53, a caretaker gene, encodes the protein p53, which is nicknamed "the guardian of the genome". p53 has many different ... There are exceptions to the two-hit rule for tumor suppressors, such as certain mutations in the p53 gene product. p53 ... Gene therapy is used to reinstate the function of a mutated or deleted gene type. When tumor suppressor genes are altered in a ... TSGs can be grouped into the following categories: caretaker genes, gatekeeper genes, and more recently landscaper genes. ...
... is a protein that in humans is encoded by the PRAL gene. "Human PubMed Reference:". National ... "Entrez Gene: P53 regulation associated lncRNA". Retrieved 2017-06-27. v t e (Articles with short description, Short description ... matches Wikidata, Human genes, All stub articles, Human chromosome 17 gene stubs). ...
These effects seem to be largely mediated by mutations at guanine in codon 249 of the p53 gene, a tumor suppressing gene, and ... us), National Center for Biotechnology Information (1998-01-01). The p53 tumor suppressor protein. National Center for ... March 2004). "Clustered pathway genes in aflatoxin biosynthesis". Appl. Environ. Microbiol. 70 (3): 1253-62. Bibcode:2004ApEnM ... at several guanine residues in the 12th and 13th codons of the ras gene, a gene whose product controls cellular proliferation ...
An example of one such gene is p53. Patients with Li-Fraumeni syndrome, for example, have mutations in the p53 gene that ... genes. In contrast to caretaker genes, gatekeeper genes encode gene products that act to prevent growth of potential cancer ... Experiments with mice that have increased gatekeeper function in the p53 gene show reduced cancer incidence (due to the ... Gatekeeper genes are in fact specific to the tissues in which they reside. The probability that mutations occur in other genes ...
Genes of the p53 family are known to be complex. The viral oncoproteins (e.g. Adenovirus E1B) that efficiently inhibit p53 ... The p73 gene encodes a protein with a significant sequence homology and a functional similarity with the tumor suppressor p53. ... The over-expression of p73 in cultured cells promotes a growth arrest and/or apoptosis similarly to p53. The p73 gene has been ... p73, also known as tumor protein 73 (TP73), protein was the first identified homologue of the tumor suppressor gene, p53. Like ...
... has been shown to interact with: C21orf7, Cyclin A1, EP300, HDAC3, NCOR1, P53, and TBL1X. GRCh38: Ensembl release ... G protein pathway suppressor 2 is a protein that in humans is encoded by the GPS2 gene. This gene encodes a protein involved in ... "Entrez Gene: GPS2 G protein pathway suppressor 2". Rual JF, Venkatesan K, Hao T, Hirozane-Kishikawa T, Dricot A, Li N, Berriz ... When overexpressed in mammalian cells, this gene could potently suppress a RAS- and MAPK-mediated signal and interfere with JNK ...
Gene knockdown is achieved by reducing the expression of a particular gene in a cell. In the case of protein-coding genes, this ... Most of these effects are due to activation of p53-mediated apoptosis and can be suppressed by co-injection of an anti-p53 ... This entire process is referred to as gene expression; it is the process by which the information in a gene, encoded as a ... a quantifiable method for gene knockdown". Genesis. 30 (3): 154-6. doi:10.1002/gene.1053. PMID 11477696. Kloosterman WP, ...
"NUMB controls p53 tumour suppressor activity". Nature. 451 (7174): 76-80. Bibcode:2008Natur.451...76C. doi:10.1038/nature06412 ... Protein numb homolog is a protein that in humans is encoded by the NUMB gene. The protein encoded by this gene plays a role in ... Four transcript variants encoding different isoforms have been found for this gene. The protein Numb is coded for by the gene, ... Among the Notch target genes are members of the HES and HEY gene families whose protein products can act as transcriptional ...
Ouchi T, Monteiro AN, August A, Aaronson SA, Hanafusa H (March 1998). "BRCA1 regulates p53-dependent gene expression". Proc. ... BRCA1 is a human tumor suppressor gene (also known as a caretaker gene) and is responsible for repairing DNA. BRCA1 and BRCA2 ... "Structure of the 53BP1 BRCT region bound to p53 and its comparison to the Brca1 BRCT structure". Genes Dev. 16 (5): 583-93. doi ... "Functional and physical interactions between BRCA1 and p53 in transcriptional regulation of the IGF-IR gene". Horm. Metab. Res ...
"BRCA1 regulates p53-dependent gene expression." (1998) Proc. Natl. Acad. Sci 95: 2302. A. August, S. Gibson, Y. Kawakami, T. ... This work was the first to show that this protein could regulate the transcription of genes and could potentially regulate the ...
... is a non-coding RNA that in humans is encoded by the LNCPRESS1 gene. GRCh38: Ensembl ... "Entrez Gene: LncRNA p53 regulated and ESC associated 1". Retrieved 2018-08-22. v t e (Articles with short description, Short ... description matches Wikidata, Orphaned articles from December 2022, All orphaned articles, Genes on human chromosome 7, All ...
Paunesku, Tatjana; Zhang, Yueru; Gemmell, M. Anne; Woloschak, Gayle E. (2000). "p53 gene deletions in radiation-induced tumors ...
Further, up-regulation of p73 (TP73), a homolog of p53, and deletion of the p53 pathway gene p14arf/p16/INK4A (CDKN2A) have ... Fink, KL; Rushing, EJ; Schold Jr, SC; Nisen, PD (1996). "Infrequency of p53 gene mutations in ependymomas". Journal of Neuro- ... While p53 (TP53) mutations are not often observed in pediatric ependymoma, the p53 pathway is suggested to play a role in ... However, gene mutations linked to the familial syndromes are rarely found in sporadic cases of ependymoma. For example, NF2 ...
This gene is induced by the tumor suppressor p53 and is thought to be involved in p53-mediated cell death. It contains a p53 ... "Entrez Gene: TP53I3 tumor protein p53 inducible protein 3". Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to ... P53 has been shown to transcriptionally activate this gene by interacting with the downstream pentanucleotide microsatellite ... 2004). "UV-dependent alternative splicing uncouples p53 activity and PIG3 gene function through rapid proteolytic degradation ...
Roth JA, Swisher SG, Meyn RE (October 1999). "p53 tumor suppressor gene therapy for cancer". Oncology. 13 (10 Suppl 5): 148-54 ... carry a balanced genetic translocation in which part of the NTRK3 gene is fused to part of the ETV6 gene to form a fusion gene ... the ER can regulate gene expression by interacting with estrogen response elements within the promotor of specific genes. The ... This fusion gene encodes a chimeric protein termed ETV6-NTRK3. The NTRK3 part of ETV6-NTRK3 protein has up-regulated tyrosine ...
Cell cycle arrest is carried out by the p53-pRb pathway. Activated p53 turns on genes for p21. P21 is a CDK inhibitor that ... Hyperphosphorylated pRb can no longer bind E2F, E2F is released and cyclin A genes, and other crucial genes for S phase, are ... Genes on human chromosome 13, Genes on human chromosome 4, Cell cycle, Proteins, Cell cycle regulators). ... Transcription of cyclin A is indirectly regulated by the tumor suppressor protein p53. P53 is activated by DNA damage and turns ...
Apoptosis-stimulating of p53 protein 1 is a protein that in humans is encoded by the PPP1R13B gene. This gene encodes a member ... They promote DNA binding and transactivation of p53-family proteins on the promoters of proapoptotic genes. Expression of this ... Hershko T, Chaussepied M, Oren M, Ginsberg D (2005). "Novel link between E2F and p53: proapoptotic cofactors of p53 are ... "Mdm2 and mdmX prevent ASPP1 and ASPP2 from stimulating p53 without targeting p53 for degradation". Oncogene. 24 (23): 3836-41. ...
"Entrez Gene: PCBP4 poly(rC) binding protein 4". Taylor WR, Stark GR (2001). "Regulation of the G2/M transition by p53". ... This gene is induced by the p53 tumor suppressor, and the encoded protein can suppress cell proliferation by inducing apoptosis ... Zhu J, Chen X (2000). "MCG10, a novel p53 target gene that encodes a KH domain RNA-binding protein, is capable of inducing ... Poly(rC)-binding protein 4 is a protein that in humans is encoded by the PCBP4 gene. This gene encodes a member of the KH ...
Armstrong, Sue (3 May 2016). P53 : the gene that cracked the cancer code. London. ISBN 978-1-4729-1052-3. OCLC 929031485.{{cite ... There, she characterized important functions of p53 needed for tumor suppression and that they were lost when p53 is mutated in ... Her research is focused on tumor suppressor protein p53 and its role as an oncogene when it is mutated in breast cancer. Born ... 1]^ Hunter, Karen (15 November 1997). "Her In-Gene-Uity Pays Work Reveals Cancer Cure". Bargonetti-Chavarria, Jill (2002-03-22 ...
... disruption of HAUSP gene stabilizes p53". Nature. 428 (6982): 1 p following 486. doi:10.1038/nature02501. PMID 15058298. S2CID ... Normally, p53 levels are kept low in part due to Mdm2-mediated ubiquitylation and degradation of p53. In response to oncogenic ... EBNA1 can compete with p53 for binding USP7. Stabilization by USP7 is important for the tumor suppressor function of p53. In ... HAUSP can deubiquitinate p53 and protect p53 from Mdm2-mediated degradation, indicating that it may possess a tumor suppressor ...
The p53 gene codes for the tumor suppressor p53 proteins. A mutation in this gene can lead to formation of tumors. Five p53 ... One mechanism by which 4-ABP causes bladder cancer is a mutation in the p53 gene, which are seen in thirty to sixty percent of ... evidence from its DNA binding spectrum in human p53 gene". Carcinogenesis. 23 (10): 1721-1727. doi:10.1093/carcin/23.10.1721. ...
This gene encodes a proline-rich protein. Studies of the related mouse gene suggest that this gene is regulated by p53 and may ... Lo PK, Chen JY, Lo WC, Chen BF, Hsin JP, Tang PP, Wang FF (Feb 2000). "Identification of a novel mouse p53 target gene DDA3". ... "Entrez Gene: PSRC1 proline/serine-rich coiled-coil 1". Kathiresan S, Melander O, Guiducci C, et al. (2008). "Six new loci ... Lo PK, Wang FF (Nov 2002). "Cloning and characterization of human and mouse DDA3 genes". Biochim Biophys Acta. 1579 (2-3): 214- ...
The AIFM2 gene contains a putative p53-binding element in intron 5, suggesting that its gene expression can be activated by p53 ... is a protein that in humans is encoded by the AIFM2 gene, also known as p53-responsive gene 3 (PRG3), on chromosome 10. This ... Wu M, Xu LG, Su T, Tian Y, Zhai Z, Shu HB (September 2004). "AMID is a p53-inducible gene downregulated in tumors". Oncogene. ... Wu M, Xu LG, Su T, Tian Y, Zhai Z, Shu HB (September 2004). "AMID is a p53-inducible gene downregulated in tumors". Oncogene. ...
"Entrez Gene: TP53BP1 tumor protein p53 binding protein 1". Bouwman P, Aly A, Escandell JM, Pieterse M, Bartkova J, van der ... Lai H, Lin L, Nadji M, Lai S, Trapido E, Meng L (2002). "Mutations in the p53 tumor suppressor gene and early onset breast ... Tumor suppressor p53-binding protein 1 also known as p53-binding protein 1 or 53BP1 is a protein that in humans is encoded by ... "Structure of the 53BP1 BRCT region bound to p53 and its comparison to the Brca1 BRCT structure". Genes & Development. 16 (5): ...
Lehmann, AR (2001). "The xeroderma pigmentosum group D (XPD) gene: One gene, two functions, three diseases". Genes & ... its aberrant association with p53 down-regulates the function of p53, leading to a reduction in p53-dependent apoptosis and ... There are 28 genes in this pathway. Individuals with defects in these genes often have developmental defects and exhibit ... All these disorders can be caused by mutations in a single gene, XPD, or in other genes. Cockayne syndrome (CS) is a rare ...
... a p53-inducible gene, regulates p53-dependent apoptosis". Mol Cell. 8 (1): 85-94. doi:10.1016/S1097-2765(01)00284-2. PMID ... Tumor protein p53-inducible nuclear protein 1 is a protein that in humans is encoded by the TP53INP1 gene. In mice this protein ... "Entrez Gene: TP53INP1 tumor protein p53 inducible nuclear protein 1". Tomasini, Richard; Samir Amina Azizi; Carrier Alice; ... Hershko T, Chaussepied M, Oren M, Ginsberg D (2005). "Novel link between E2F and p53: proapoptotic cofactors of p53 are ...
"Entrez Gene: P53-responsive gene 1". Retrieved 2017-11-07. Ozalp S, Yalcin OT, Tanir HM, Kabukcuoglu S, Erol G (2003). "p53 ... P53-responsive gene 1 is a protein that in humans is encoded by the PRG1 gene. "Human PubMed Reference:". National Center for ... Human genes, All stub articles, Human chromosome 19 gene stubs). ... "P53 and K-ras mutations are frequent events in microscopically ...
The Lozano Lab at MD Anderson main research study is on the mutation of p53 protein genetics and the elaboration of tumors. ... Mutation of the p53 gene is a critical event in the elaboration of many tumors of diverse origin. The p53 protein is activated ... Alterations in components of the p53 pathway, such as amplification of the Mdm2 gene, which encodes a p53 inhibitor, also ... Lozano was the first to establish p53 as a transcriptional activator of other genes. She also showed that common p53 mutants ...
... which encodes a p53-associated protein. SSCP (single-strand conformation polymorphism) analysis and direct sequencing of ... In this study we have screened a series of 29 primary leiomyosarcomas for abnormalities of both the p53 gene and the MDM2 gene ... In this study we have screened a series of 29 primary leiomyosarcomas for abnormalities of both the p53 gene and the MDM2 gene ... When considered together, these results indicate that alterations in both the p53 gene and MDM2 gene are important in the ...
If p53 is inactivated, as it is in over half of all human cancers, checks and balances on cell growth fail to operate, and body ... The cellular cascade of molecular signals that instructs cells with fatally damaged DNA to self-destruct pivots on the p53 ... Study causes big shift in how we think about p53 gene. *Download PDF Copy ... But when the cell senses that its DNA has been damaged, it slows down the degradation of p53, so that p53 protein levels can ...
CDIP1 cell death inducing p53 target 1 [Homo sapiens] CDIP1 cell death inducing p53 target 1 [Homo sapiens]. Gene ID:29965 ... Gene neighbors Overlapping genes and two nearest non-overlapping genes on either side ... cell death-inducing p53-target protein 1. Names. LITAF-like protein. cell death inducing protein. cell death involved p53- ... CDIP1 cell death inducing p53 target 1 [ Homo sapiens (human) ] Gene ID: 29965, updated on 7-Sep-2023 ...
Although p53 The Gene That Cracked the Cancer Code by Sue Armstrong conveys the details that led up to a great discovery, the ... Be the first to review "p53: The Gene that Cracked the Cancer Code" Cancel reply. Your email address will not be published. ... Home / Non-Fiction / Science & Nature / p53: The Gene that Cracked the Cancer Code. ... which alludes to tobacco smoking and how its toxins affect the p53 gene. I believe the author is trying to support the research ...
... and anti-cancer wild-type p53 gene (wt-p53), was presented in our former studies (Int J Nanomedicine 8:3757-68, 2013, Liver Int ... with the objective of understanding their roles in hepatoma TAE-gene therapy. In vitro, L-nanoplex managed the highest gene ... In vivo, being the only one with successful gene transference to hepatic VX2 tumor, Pll-nanoplex/lipiodol emulsion can target ... L-nanoplex respectively with wt-p53 expressing plasmid. The four nanoplexs were then applied in vitro for human normal hepacyte ...
... ... DNA from 123 lung cancers specimens and corresponding normal tissue were used and evaluated by Sanger sequencing of the p53 ... Science for Life Laboratory, School of Biotechnology, Division of Gene Technology, Royal Institute of Technology, Stockholm, ... Science for Life Laboratory, School of Biotechnology, Division of Gene Technology, Royal Institute of Technology, Stockholm, ...
Through cloning of functional p53-binding sites (p53-tagged sites) from the human genome, we isolated a novel gene inducible by ... Cloning of P2XM, a Novel Human P2X Receptor Gene Regulated by p53 Tsutomu Urano; Tsutomu Urano ... a Novel Human P2X Receptor Gene Regulated by p53. Cancer Res 1 August 1997; 57 (15): 3281-3287. ... Hence, we designated the gene P2XM (P2X specifically expressed in skeletal muscle). P2XM was localized to chromosomal band ...
The Investigation of p53 and Ki-67 Gene Mutations in Relation with Helicobacter pylori Infection in Patients with Gastric ... The Investigation of p53 and Ki-67 Gene Mutations in Relation with Helicobacter pylori Infection in Patients with Gastric ... The Investigation of p53 and Ki-67 Gene Mutations in Relation with Helicobacter pylori Infection in Patients with Gastric ... The aim of this study was to evaluate the role of Helicobacter pylori infection in relation with p53 and Ki-67 mutations in a ...
The activity of the p53 gene product is regulated by a plethora of posttranslational modifications. An open question is whether ... Characterization of the gene-expression pattern elicited by p53 acetylation mutants. (A) Clustering of genes regulated by p53 ... Characterization of the gene-expression pattern elicited by p53 acetylation mutants. (A) Clustering of genes regulated by p53 ... Genes containing putative p53 consensus sites and relative scores are shown. Gene length represents the combined base-pair ...
This study was designed to investigate the association of gene polymorphisms in the p53 gene and mitochondrial genome D-loop ... Objective: This study aims to investigate the association of p53 and D-loop gene with drug resistance and sensitization induced ... Association of p53 and mitochondrial gene with chemosensitization by metformin in ovarian cancer. ... we screened the potential indicators for forecasting of metformin sensitivity using p53 and mitochondrial D-loop region gene ...
We show that MDCK cells silenced for the polarity gene scribble (scribKD) are hypersensitive to compaction, that interaction ... Compaction, via activation of Rho-associated kinase (ROCK) and the stress kinase p38, leads to further p53 elevation, causing ... Given the involvement of p53, compaction hypersensitivity may be widespread among damaged cells and offers an additional route ... Importantly, we show that elevation of the tumour suppressor p53 is necessary and sufficient for crowding hypersensitivity. ...
TP63 is a member of the tumour suppressor TP53 gene family, and ΔNp63α, a ... ... This may be because cell cycle arrest-related genes can be regulated by genes other than p53. Consistent with this model, the ... or to gene expression regulated by ΔNp63α will require further discussion addressing a wider range of p53-related genes. ... has been thought to work competitively with p53 against target genes, thereby inhibiting the typical function of p53. On the ...
The P53 gene and response of colorectal tumours to adjuvant therapy. *Iacopetta, Barry (Chief Investigator) ...
... highlighting the role of the P53-mTOR pathway in this context. Overall, we have constructed an atlas of essential and growth- ... we generated a genome-wide loss-of-function library targeting 18,166 protein-coding genes to define the essential genes in ... hPSC-enriched essential genes mainly encode transcription factors and proteins related to cell-cycle and DNA-repair, revealing ... Our screen also led to the identification of growth-restricting genes whose loss of function provides a growth advantage to ...
... Guido T. Bommer, Isabelle Gerin, Ying Feng, Andrew J. ... p53-Mediated Activation of miRNA34 Candidate Tumor-Suppressor Genes. , Current Biology, August 2007, Elsevier, DOI: 10.1016/j. ...
So to keep it simple, I will focus on one particular gene expression called P53. When this gene is working correctly, it helps ... When the P53 gene is working correctly, it helps protect against pathogenic mutations of all kinds. When it goes awry, however ... What You Can Do to Support Your P53 Genes There are a lot of things you can do to ensure that all of your genes are working for ... How the P53 Gene Becomes Mutated When P53 is working properly, it becomes most active when acute stress occurs. When this ...
The Tobacco-Related Disease Research Program (TRDRP) funds research that enhances understanding of tobacco use, prevention and cessation, the social, economic and policy-related aspects of tobacco use, and tobacco-related diseases in the State of California.
We have obtained a 20-gene signature whose genes are overexpressed in mouse tumors and can identify human tumors with poor ... Two of the genes of this signature, AURKA and UBE2C, were validated in human breast and cervical cancer as potential biomarkers ... Since alterations of p53-dependent pathway are common hallmarks of aggressive, poor prognostic human cancers, these mouse ... Remarkably, they are also enriched in human embryonic stem cell gene signatures, a characteristic feature of human aggressive ...
A diagram showing the major cancer genes for some cancers. The larger the ... The protein and its corresponding gene were named p53, in reference to the mass of the protein (53 kilodaltons). The p53 gene ... Cancer Genes A diagram showing the major cancer genes for some cancers. The larger the gene name, the more frequently that gene ... p53 was kept active by removing the MDM2 gene from mice. MDM2 causes the inactivation of p53, so when it is gone, p53 can ...
Genes, Patents, and Race: The History of Science as a Bridge Between Disciplines on Friday, October 26 at 5:30 p.m. in ... The p53 Protein: From Cell Regulation to Cancer Edited by Arnold J. Levine ... As part of this lecture, he will discuss his role with the ACLU in opposing breast cancer gene patents in a case that went to ... Myles W. Jackson to Confront Questions of Genes, Patents, and Race in Debut IAS Public Lecture Panel Discussion to Feature ...
p53 is a very versatile gene that controls many tumor-suppressing functions. What are some of the specific functions it ... p53 is a very versatile gene that controls many tumor-suppressing functions. What are some of the specific functions it ... p53 is a very versatile gene that controls many tumor-suppressing functions. September 13, 2022. /0 Comments/in Nursing /by ... 33p53 is a very versatile gene that controls many tumor-suppressing functions.. ...
... a novel human P2X receptor gene regulated by p53. ... Through cloning of functional p53-binding sites (p53-tagged ... Cloning of P2XM, a novel human P2X receptor gene regulated by p53. ... Cloning of P2XM, a novel human P2X receptor gene regulated by p53. ... we isolated a novel gene inducible by wild-type p53. Its cDNA sequence contained an open reading frame encoding a 431-amino ...
p53 gene mutations. Individuals diagnosed with cancer. Predictive for treatment. Cancer. PIK3CA mutations. Persons with cancer ... Gene ratio test for four genes. 1) persons suspected of having mesothelioma 2) Mesothelioma patients. 1) Diagnosis and 2) ... gene expression. Persons with suspected lung cancer. Diagnosis of lung cancer. Lung Cancer. PI3K. Patients suffering from lung ... Gene Expression. Heart Transplant Patients. Risk Assessment for low/moderate ACR. Acute Lymphoblastic Leukemia (ALL). TPMT. ...
... ... To cite: Boominathan, p53/p63/p73 inhibits generation of glioma stem cells through its target genes , 27/December/2012, Genome- ...
... ts-p53) when cells are shifted down to 32.5 degrees C, a temperature at which ts-p53 possesses wild-type (wt)-like activities. ... which exhibits enhanced binding to temperature-sensitive p53 ( ... suggest that the mdm2 gene is a target for activation by wt p53 ... We have recently characterized a 95 kDa protein, p95, which exhibits enhanced binding to temperature-sensitive p53 (ts-p53) ... suggesting a direct involvement of p53 in the process. Based on these data and on recent findings implicating p53 as a ...
Here, we report the generation of highly efficient, heritable gene knockouts at two clock gene loci, and knockout, thereby ... The eastern UNITED STATES monarch butterfly, functional analysis of candidate genes. The eastern UNITED STATES monarch ... Furthermore, our and data showed a synergistic anticancer effect of chemical inhibitors for specific genes in these two ... In fact, zinc-finger nucleases possess allowed heritable targeted mutagenesis of the monarch clock gene previously, (2013). ...
  • SSCP (single-strand conformation polymorphism) analysis and direct sequencing of polymerase chain reaction (PCR)-amplified DNA were used to establish that 6/29 tumours possessed point mutations of the p53 gene. (nih.gov)
  • Using a monoclonal antibody that recognises the p53 protein in immunohistochemical staining experiments, we observed overexpression of the p53 protein in five of the six tumours containing point mutations in the p53 gene. (nih.gov)
  • If p53 is inactivated, as it is in over half of all human cancers, checks and balances on cell growth fail to operate, and body cells start to accumulate mutations, which ultimately may lead to cancer. (news-medical.net)
  • Short p53 inhibition improved the yield of edited cells without hurting genome stability or increasing mutations, they reported. (fiercebiotech.com)
  • The aim of this study was to evaluate the role of Helicobacter pylori infection in relation with p53 and Ki-67 mutations in a case-control study in Iran, an endemic region for H. pylori infection. (scialert.net)
  • Age, sex, H. pylori serology and presence of p53 and Ki-67 mutations were determined for all subjects. (scialert.net)
  • However, there are few studies on the relationship between gene mutations in these two and the sensitization of ovarian cancer. (oncotarget.com)
  • When this gene is working correctly, it helps protect against pathogenic mutations of all kinds. (breastcancerconqueror.com)
  • The most extreme P53 mutations, however, will be found when it comes to cancer. (breastcancerconqueror.com)
  • When this stress is prolonged or even ongoing P53 becomes taxed and mutations in its function begin. (breastcancerconqueror.com)
  • For example, some experts have found that Herpes Virus 6 can attack P53 and lead to mutations. (breastcancerconqueror.com)
  • A connection may also exist between radiation/ EMF overexposure and P53 mutations. (breastcancerconqueror.com)
  • ALL cancers have lots of additional changes, the so-called 'passenger' mutations, that may contribute to the cancer, but are not the main genes. (cancerquest.org)
  • On average, we identify 43 mutations per tumour, excluding four cases with a mutator phenotype that harboured inactivating mutations in mismatch repair genes. (nih.gov)
  • In addition to mutations in TP53 and KRAS, we identify genetic alterations in chromatin remodelling genes, ARID1A and ARID1B, in histone methyltransferase MLL3, in histone deacetylase modifier SPOP and in chromatin assembly factor BAZ1A, in nearly two thirds of cases. (nih.gov)
  • There are only 12 known mutations of the reported type, and the finding of such a rare mutational event in a low-incidence p53 mutation tumor, such as SPNET, might add additional insight into the p53-SPNET relationship in tumorigenesis. (tau.ac.il)
  • Although not widely accepted, it is possible that different mutations of the p53 gene in patients with brain tumors may imply a different ultimate prognosis. (tau.ac.il)
  • In contrast to the early expression of CD44 in small adenomas, mutations of K-ras and p53 were detected preferentially in large adenomas and late-stage adenomas containing carcinoma. (johnshopkins.edu)
  • Mutations in p53, found in most cancers, lead to uncontrollable cell division. (medscape.com)
  • Goldberg said, "Preliminary studies have shown responses in sarcoma patients with P53 mutations. (medscape.com)
  • Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families such as Li-Fraumeni syndrome. (thermofisher.com)
  • At least 44 RPL11 gene mutations have been identified in individuals with Diamond-Blackfan anemia. (medlineplus.gov)
  • The RPL11 gene mutations that cause Diamond-Blackfan anemia are believed to cause problems with ribosomal function. (medlineplus.gov)
  • Cmejla R, Cmejlova J, Handrkova H, Petrak J, Petrtylova K, Mihal V, Stary J, Cerna Z, Jabali Y, Pospisilova D. Identification of mutations in the ribosomal protein L5 (RPL5) and ribosomal protein L11 (RPL11) genes in Czech patients with Diamond-Blackfan anemia. (medlineplus.gov)
  • Germline mutations in the p53 tumor suppressor gene are associated with the Li-Fraumeni syndrome, characterized by childhood sarcoma, leukemia and early onset breast cancer and has occasionally been found also in familial breast-ovarian cancer. (lu.se)
  • Most mutations found are of missense type and located in the central region of the gene (exons 5 to 8). (lu.se)
  • The overall goal of my laboratory is to understand the signals that regulate the p53 pathway and the consequences of expressing wild-type or mutant p53. (mdanderson.org)
  • A University of Wisconsin-Madison team recently identified an enzyme that helps mutant p53 accumulate and therefore promote aggressive cancers. (fiercebiotech.com)
  • New Jersey biotech PMV Pharma , a 2017 FierceBiotech Fierce 15 company, is also working on small molecules that could correct mutant p53. (fiercebiotech.com)
  • The effect of p53 gene therapy on chemosensitivity and apoptotic response of PANC-1 tumor cells, which express high amount of mutant p53, to cancer chemotherapeutic agents of Etoposide and Doxorubicin was investigated. (ijbiotech.com)
  • This evidence reinforce the view that combining p53 gene therapy with conventional chemotherapeutic agents may yield a more beneficial response than conventional treatments alone in pancreatic tumor cells with high amount of mutant p53. (ijbiotech.com)
  • The antibody should recognize human wild-type and mutant p53. (abcam.com)
  • She also showed that common p53 mutants fail to launch transcription, and discovered other proteins, Mdm2 and Mdm4, which play critical roles in inhibiting p53 activity in development and cancer. (mdanderson.org)
  • When higher than normal levels of p53 tumor suppressor exist, there is enough p53 to bind to many regulatory sites in the cell's genome to activate the production of other proteins that will halt cell division if the DNA damage can be repaired. (news-medical.net)
  • After irradiation, the expression of DDR-related genes and proteins in ΔNp63α-expressing and control cells was analysed by RT-qPCR, Western blotting, and flow cytometry. (researchsquare.com)
  • hPSC-enriched essential genes mainly encode transcription factors and proteins related to cell-cycle and DNA-repair, revealing that a quarter of the nuclear factors are essential for normal growth. (nature.com)
  • P53 produces proteins that repair damaged cells. (breastcancerconqueror.com)
  • Note that by convention gene names are italicized and the proteins they make are not. (cancerquest.org)
  • The fairly divergent P gene [5-7] encodes a multifunctional phosphoprotein (P proteins) [8] and continues to be extensively looked into using lab modified RABV strains. (techuniq.com)
  • This gene is located in a cluster of closely related salivary proline-rich proteins on chromosome 12. (cancerindex.org)
  • p53 is up-regulated in response to stress signals and stimulated to activate transcription of specific genes, resulting in expression of p21waf1 and other proteins involved in G1 or G2/M arrest. (thermofisher.com)
  • The RPL11 gene provides instructions for making one of approximately 80 different ribosomal proteins, which are components of cellular structures called ribosomes. (medlineplus.gov)
  • Haploinsufficiency of ribosomal proteins and p53 activation in anemia: Diamond-Blackfan anemia and the 5q- syndrome. (medlineplus.gov)
  • 2 cases of EBV-LMPI protein expression did not express p53 protein and 7 cases did not express both p53 and EBV-LMPI proteins. (bvsalud.org)
  • Mutation of the p53 gene is a critical event in the elaboration of many tumors of diverse origin. (mdanderson.org)
  • Except for evidence of a rearrangement in a single leiomyosarcoma cell line, SK-UT-1, we have found no direct evidence to support a role for mutation of the gene in the development of human soft-tissue tumours. (nih.gov)
  • According to many studies , P53 mutation are found in half of all human cancers. (breastcancerconqueror.com)
  • What specific factors can lead to P53 mutation? (breastcancerconqueror.com)
  • A 2002 study conducted by a joint UK-Italian research team found that Breast Cancer patients who have P53 mutation suffered from more aggressive forms. (breastcancerconqueror.com)
  • In this study we examined the relationship of CD44 expression to somatic genetic events in the adenoma-carcinoma sequence: point mutation of K-ras in codons 12 and 13 and overexpression of p53 protein as a marker of gene mutation. (johnshopkins.edu)
  • CD44 was absent in the other 2 small adenomas positive for K-ras mutation or p53 overexpression. (johnshopkins.edu)
  • The frequent expression of CD44 prior to K-ras and p53 gene alterations in colorectal neoplasia suggests that activation of CD44 gene expression is related to earlier events in the adenoma-carcinoma sequence, possibly cell activation and proliferation following APC gene mutation or alteration of DNA methylation. (johnshopkins.edu)
  • The family manifested no linkage to the p53 gene (a two-point LOD-score of -0.41), and has previously also been excluded for linkage to the BRCA1 and BRCA2 loci, as well as being carrier of a BRCA1 germline mutation. (lu.se)
  • Although it seems unlikely that the p53 germline mutation is the major cause of disease predisposition in Lund 5, the data suggest that some p53 alteration may confer a subtle influence on breast cancer development and progression. (lu.se)
  • In about half of human cancers, p53 is inactivated through DNA mutation. (who.int)
  • Recently, we identified TRIM22 as a novel p53 target gene and showed that overexpression of TRIM22 inhibits the clonogenic growth of monoblastic U937 cells. (lu.se)
  • Sometimes called the 'guardian of the genome,' p53 is a tumor suppressor gene that, when neutralized, plays a critical role in the development of many types of tumors. (mdanderson.org)
  • Known as "the guardian of the genome," the p53 gene helps stabilize DNA and prevent cancer formation. (fiercebiotech.com)
  • Validation of whole genome amplification for analysis of the p53 tumor suppressor gene in limited amounts of tumor samples. (diva-portal.org)
  • Through cloning of functional p53-binding sites (p53-tagged sites) from the human genome, we isolated a novel gene inducible by wild-type p53. (aacrjournals.org)
  • This study was designed to investigate the association of gene polymorphisms in the p53 gene and mitochondrial genome D-loop region with metformin-induced sensitization and prognosis of ovarian cancer. (oncotarget.com)
  • Using our recently established haploid human pluripotent stem cells (hPSCs), we generated a genome-wide loss-of-function library targeting 18,166 protein-coding genes to define the essential genes in hPSCs. (nature.com)
  • Of the 30,000 or so genes that are currently thought to exist in the human genome , there is a small subset that seems to be particularly important in the prevention, development, and progression of cancer. (cancerquest.org)
  • The distinctively mapped brief reads were utilized to identify parts of the genome with significant enrichment in p53-connected DNA sequences. (healthweeks.com)
  • RABV includes a non-segmented harmful feeling RNA genome made up of five genes in the purchase 3-N-P-M-G-L-5 [4]. (techuniq.com)
  • Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukaemia. (cancerindex.org)
  • Here, we further examined the gene expression profile by using genome microarrays to profile molecular mechanisms of SWCNT oncogenesis. (cdc.gov)
  • Phosphorylation of Ser392 in p53 has been shown to associate with the formation of human tumors. (thermofisher.com)
  • p53, mdm-2, p21, and mib-1 expression were assessed by immunohistochemical methods in primary tumors derived from 134 patients who took part in a randomized multicenter trial comparing docetaxel to sequential methotrexate and 5-fluorouracil (MF) in advanced breast cancer. (lu.se)
  • Interestingly, tumors with both negative mdm-2 and p21 expression, irrespective of p53 status, had a high response rate to docetaxel but no response to MF. (lu.se)
  • Loss of heterozygosity at the p53 locus was not seen in the primary tumors of these women, but appeared as a partial loss of the wildtype allele in subsequent recurrent lesions of two gene carriers. (lu.se)
  • Alterations in components of the p53 pathway, such as amplification of the Mdm2 gene, which encodes a p53 inhibitor, also contribute to tumorigenesis. (mdanderson.org)
  • Dr. Lozano is recognized as a pioneer in describing the p53 pathway, a recognized tumor suppressor gene associated with cancer. (mdanderson.org)
  • Guillermina's pioneering work in genetics has paved the way for innovative research at MD Anderson and at cancer centers around the world," said President Peter WT Pisters, M.D. "We are proud to count her among our most distinguished faculty, and we are excited to see her recognized by our peers for her transformative work in outlining the p53 pathway. (mdanderson.org)
  • Lozano has been elected to the National Academy of Sciences (NAS) for her pioneering work in describing the p53 pathway, a recognized tumor suppressor gene associated with cancer. (mdanderson.org)
  • Many chemotherapeutical drugs used to treat cancer exert their biological effects on tumor cells through activation of the p53 pathway. (news-medical.net)
  • Acts upstream of or within intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator and tumor necrosis factor-mediated signaling pathway. (nih.gov)
  • Our screen also led to the identification of growth-restricting genes whose loss of function provides a growth advantage to hPSCs, highlighting the role of the P53-mTOR pathway in this context. (nature.com)
  • In response to DNA-damaging agents, the wild-type p53-activated fragment 1 (WAF1 also known as p21) is an important downstream effector in the p53-specific growth arrest pathway. (lu.se)
  • However, WSC induced cell cycle arrest and cellular senescence mediated by the p53-p21 pathway. (who.int)
  • Instead of accumulating in mouse cells and halting cell division in the genetically engineered mice, the altered p53 protein performed flawlessly: it was unstable when no DNA damage was present and was stable and fully functional when needed to halt the cycle cell to repair DNA damage or to induce apoptosis. (news-medical.net)
  • Expression of the p53 target CDIP correlates with sensitivity to TNFα-induced apoptosis in cancer cells. (nih.gov)
  • In the process of apoptosis, mitochondria are a regulation object of p53 and an important participant in the energy metabolism in cells. (oncotarget.com)
  • If it cannot be repaired, P53 will signal for the cell to undergo apoptosis, or cancer cell death. (breastcancerconqueror.com)
  • Furthermore, treatment of both PANC-1 cells as well as its wt-p53 transfectants with etoposide resulted in apoptosis despite the difference in their p53 status, although, the number of apoptotic cells of the wt-p53 transfectants was higher compared to the control cells. (ijbiotech.com)
  • We also discovered that prohibitin and prohibiton up-regulated transcription 3rd party of p53 although p53 certainly enhanced this technique which the knock-down of prohibitin and prohibiton inhibited camptothecin-induced apoptosis. (biotech-angels.com)
  • Based on differentially expressed genes, possible mechanisms of SWCNT-associated apoptosis resistance and oncogenesis were identified, which included activation of pAkt/p53/Bcl-2 signaling axis, increased gene expression of Ras family for cell cycle control, Dsh-mediated Notch 1, and downregulation of apoptotic genes BAX and Noxa. (cdc.gov)
  • p53 mediates cell cycle arrest or apoptosis in response to DNA damage or starvation for pyrimidine nucleotides. (thermofisher.com)
  • p53 is a transcription factor that participates in cell cycle checkpoint processes and apoptosis. (lu.se)
  • The p53 protein is activated in response to DNA damage, serving as a checkpoint in the elimination or repair of cells with damaged DNA. (mdanderson.org)
  • After screening different histone lysine methyltransferases and demethylases, we identified JMJD2B/KDM4B as a p53-inducible gene in response to DNA damage. (escholarship.org)
  • When considered together, these results indicate that alterations in both the p53 gene and MDM2 gene are important in the development of a significant minority of leiomyosarcomas. (nih.gov)
  • Alterations in genes with potential clinical utility are observed in more than three quarters of the cases and included members of the PI3-kinase and homologous DNA repair pathways. (nih.gov)
  • Neoplastic progression of colorectal epithelial cells from benign adenomas to malignant carcinomas appears to result from a series of genetic alterations involving both oncogenes and tumor suppressor genes. (johnshopkins.edu)
  • Alterations of p53, cyclinD1, Rb, and H-ras in human oral carcinomas related to tobacco use. (bvsalud.org)
  • A new mouse model, created by scientists at the Salk Institute for Biological Studies , suggests that what researchers have learned about the regulation of p53 activity from in vitro studies may not be relevant to living, breathing organisms. (news-medical.net)
  • The protein product of the murine double minute gene 2 (mdm-2) plays a central role in the regulation of p53. (lu.se)
  • Given the involvement of p53, compaction hypersensitivity may be widespread among damaged cells and offers an additional route to eliminate unfit cells. (nature.com)
  • The induction occurs with very rapid kinetics and does not require de novo protein synthesis, suggesting a direct involvement of p53 in the process. (nih.gov)
  • Southern analysis of tumour DNA revealed that 2/29 tumours demonstrated amplification of the MDM2 gene. (nih.gov)
  • TP63 is a member of the tumour suppressor TP53 gene family, and ΔNp63α, a TP63 splicing variant, is constitutively expressed in the stem cell-containing basal layer of stratified epithelial tissues, including the mammary gland, where it plays a critical role in stemness and tissue development. (researchsquare.com)
  • DNA from 123 lung cancers specimens and corresponding normal tissue were used and evaluated by Sanger sequencing of the p53 exons 5-8. (diva-portal.org)
  • A diagram showing the major cancer genes for some cancers. (cancerquest.org)
  • Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and cause the loss of tumor suppressor activity. (thermofisher.com)
  • The other half of cancers harbour a wild-type p53 gene whose tumour suppressor functions are altered by different mechanisms, which are not yet completely understood. (who.int)
  • Hagi-Sharifia Taghavi, M., Mirshahi, M., Davoodi, J. Wild type p53 gene transfer increases chemosensitivity and apoptotic response of PANC-1 pancreatic tumor cell line. (ijbiotech.com)
  • proven that prohibitin and prohibiton from the (TGYCC)15 theme whatever the p53 position and apoptotic tension. (biotech-angels.com)
  • It has recently been reported that Madin-Darby canine kidney (MDCK) epithelial cells silenced for the polarity gene scribble ( scrib KD cells) are eliminated in the presence of wild-type MDCK cells 23 , while they are viable on their own 23 . (nature.com)
  • To elucidate the role of the p53-repressive effect of ΔNp63α in radiation response, we performed a p63-siRNA knockdown experiment using human mammary epithelial cells (HMECs) expressing ΔNp63α and then performed ectopic and entopic expression experiments using human induced pluripotent stem cells (hiPSCs). (researchsquare.com)
  • Gene expression profile of human lung epithelial cells chronically exposed to single-walled carbon nanotube s. (cdc.gov)
  • p53 positivity was looked for in each IHC stained slide and the number of positive cells amongst 1,000 epithelial cells were recorded. (bvsalud.org)
  • The expression of p53 in epithelial hyperkeratosis was mainly localized to basal epithelial cells whereas in epithelial dysplasia, it was predominantly localized to spinous epithelial cells. (bvsalud.org)
  • We have also examined the role of the DCC tumour-suppressor gene in the development of human soft-tissue tumours in a variety of histological types. (nih.gov)
  • Computer based image analysis of immunohistochemical expressions of p53 and p21 was investigated in 18 samples of OLP, 10 normal oral epithelium (NOE), 10 oral squamous cell carcinoma (OSCC), 13 OM, 20 oral focal keratosis (OFK), and 30 samples of oral epithelial dysplasia (OED). (bvsalud.org)
  • Two contiguous sections from 30 tissue specimens (10 each from oral hyperplastic epithelium, dysplastic epithelium and squamous cell carcinoma) were subjected to hematoxylin and eosin (H/E) staining for histopathological diagnosis and immunohistochemical (IHC) staining for demonstration of p53. (bvsalud.org)
  • The following product was used in this experiment: P53 Monoclonal Antibody (5B10) from Thermo Fisher Scientific, catalog # BSM-33209M. (thermofisher.com)
  • Polymerase chain reaction-single strand conformation polymorphism analysis of all p53 exons was performed, and a unique variant of a transversion at codon 179 of exon 5 was revealed. (tau.ac.il)
  • Until now, many scientists thought that specific modifications on the easily accessible tail end, or C-terminus, of the p53 protein are crucial for both, timely degradation or activation. (news-medical.net)
  • So the researchers used nuclease that is highly specific to make the Cas9 scissors more precise and thus limit p53 activation. (fiercebiotech.com)
  • The brief p53 activation only delayed HSPC proliferation, rather than stopping it, and that delay could be overcome by transiently inactivating the p53 response during gene editing, the researchers found. (fiercebiotech.com)
  • These findings indicate that JMJD2B acts in an auto-regulatory loop by which p53, through JMJD2B activation, is able to influence its own transcriptional program. (escholarship.org)
  • Compaction, via activation of Rho-associated kinase (ROCK) and the stress kinase p38, leads to further p53 elevation, causing cell death. (nature.com)
  • Specifically, we show that scrib KD cells' compaction causes activation of the Rho-associated kinase (ROCK), which in turn activates p38 leading to further p53 elevation and cell death. (nature.com)
  • Based on these data and on recent findings implicating p53 as a transcription factor, we suggest that the mdm2 gene is a target for activation by wt p53. (nih.gov)
  • There are various phosphorylation sites on p53, of which the phosphorylation at Ser15 is important for p53 activation and stabilization. (thermofisher.com)
  • Specifically, UVB irradiation leads to p53 transcriptional activation of ghrelin in skin adipocytes, while a conditional p53-knockout in mice abolishes UVB-induced ghrelin expression and food-seeking behavior. (reddit.com)
  • Transcription factors (TFs) are critical for B-cell differentiation, affecting gene expression both by repres- sion and transcriptional activation. (lu.se)
  • Capitalizing on crystal structure information obtained from a previous effort in the search for non peptide inhibitors of the p53-MDM2 interaction, we have discovered another new class of compounds able to disrupt this protein-protein interaction, an important target in oncology drug research. (rcsb.org)
  • In this study we have screened a series of 29 primary leiomyosarcomas for abnormalities of both the p53 gene and the MDM2 gene, which encodes a p53-associated protein. (nih.gov)
  • HER2/neu (also called ERB B2 ) is the gene that encodes the human epidermal growth factor receptor type 2. (cancerquest.org)
  • This gene encodes a member of the heterogeneous family of basic, proline-rich, human salivary glycoproteins. (cancerindex.org)
  • In addition, we have demonstrated a significant association between the presence of abnormalities of the p53 gene or MDM2 genes in leiomyosarcomas and a more advanced clinicopathological stage (P = 0.03). (nih.gov)
  • In the last decade, diagnostic and prognostic evaluation has been facilitated by global gene expression profiling (GEP), provid- ing a new powerful means for the classification, prediction of survival, and response to treatment of lym- phomas. (lu.se)
  • Prognostic significance of p53 expression in oral squamous cell carcinoma without neck node metastases. (bvsalud.org)
  • The enhanced complex formation of mdm2 with ts-p53 in cells maintained at 32.5 degrees C is due to an elevation in total mdm2 protein levels following the temperature shift. (nih.gov)
  • We further demonstrate that the induction of mdm2 expression by t p53 activity is at the mRNA level. (nih.gov)
  • In view of the ability of mdm2 to act as a specific antagonist of p53 activity, this induction process may serve to tightly autoregulate p53 activity in living cells. (nih.gov)
  • An appropriate strategy has allowed us to translate the high biochemical potency in significant anti-proliferative activity on a p53-dependent MDM2 amplified cell line. (rcsb.org)
  • Differential gene activity is controlled by transcription factors but also dependent on the underlying chromatin structure, especially on covalent histone modifications. (escholarship.org)
  • Promoter Evaluation Chip-Seq Data Evaluation Chromatin Immunoprecipitation To recognize putative p53 binding sites in genomic series we used a posture weight matrix technique [43]. (healthweeks.com)
  • In females, estrogen interferes with the p53-chromatin interaction on the ghrelin promoter, thus blocking ghrelin and food-seeking behavior in response to UVB exposure. (reddit.com)
  • Although we detected no genetic alteration in the coding sequences, one of four rhabdomyosarcoma cell lines examined had completely lost expression of this gene. (aacrjournals.org)
  • Functionally, exogenous expression of JMJD2B enhanced subcutaneous tumor growth of colon cancer cells in a p53-dependent manner, and genetic inhibition of JMJD2B impaired tumor growth in vivo. (escholarship.org)
  • Background While the function from the phosphoprotein (P) gene from the rabies virus (RABV) continues to be well studied in lab adapted RABVs, the genetic evolution and diversity characteristics from the P gene of street RABVs remain unclear. (techuniq.com)
  • Keywords: Rabies computer virus, Phosphoprotein gene, Genetic diversity, Molecular evolution Introduction Rabies is usually a lethal neurological disease caused by infection with members of the genus lyssavirus . (techuniq.com)
  • These studies provide new insights into the regulatory effect exerted by JMJD2B on tumor growth through the modulation of p53 target genes. (escholarship.org)
  • The cellular cascade of molecular signals that instructs cells with fatally damaged DNA to self-destruct pivots on the p53 tumor suppressor gene. (news-medical.net)
  • Until now, scientists had assumed, based on studies in cultured cells, that p53 had to be modified by attaching chemical groups to specific sites on the protein to function normally in the body. (news-medical.net)
  • Since the p53 protein is able to trigger such drastic action as cellular suicide, the cells of the body must ensure that the p53 protein is only activated when damage is sensed and that the protein is quickly degraded when it is not needed. (news-medical.net)
  • As it turns out, the DNA double-stranded breaks induced by CRISPR "scissors" such as the Cas9 enzyme could activate p53, which then prevents the edited hematopoietic stem and progenitor cells (HSPCs) from proliferating. (fiercebiotech.com)
  • That off-target effect can in turn increase p53 activity and ultimately kill the edited cells. (fiercebiotech.com)
  • And with that technique, the p53 response "appears to be fully reversible and compatible with maintenance of the important biological properties of the hematopoietic stem cells," Luigi Naldini, a study co-senior author, said in a statement. (fiercebiotech.com)
  • We show that MDCK cells silenced for the polarity gene scribble ( scrib KD ) are hypersensitive to compaction, that interaction with wild-type cells causes their compaction and that crowding is sufficient for scrib KD cell elimination. (nature.com)
  • We find that scrib KD cells are hypersensitive to compaction and that this is due to elevation of baseline p53 levels, which is both necessary and sufficient to induce hypersensitivity to crowding and confer a mechanical loser status. (nature.com)
  • Overall, this work demonstrates that mechanical forces can be responsible for the elimination of cells during cell competition and that p53 levels play a key role both in instructing the mechanical loser status and in the execution of mechanical cell competition. (nature.com)
  • This p53-repressive activity may cause genomic instability in epithelial stem cells exposed to radiation. (researchsquare.com)
  • Transcriptomic analysis showed decreased RNA expression of cell cycle-related genes and increased expression of programmed cell death-related genes in sip63 cells compared to scr cells. (researchsquare.com)
  • Taken together, these results indicate that ΔNp63α represses p53-related radiation-induced DDR, thereby potentially causing genomic instability in epithelial stem cells. (researchsquare.com)
  • The DNA guardian protein p53 plays the most important role in DDR: it promotes DNA repair and the elimination of cells that are unable to repair the damage caused by oxidative stresses, including radiation. (researchsquare.com)
  • P53 is similar to the BCRA gene in that, when it is working properly, it actually protects against the excessive growth of cancer cells. (breastcancerconqueror.com)
  • When P53 senses that there is some kind of stressor, that cells are dividing too fast or that there is some other kind of irregularly, this is when it springs into action. (breastcancerconqueror.com)
  • Genes whose protein products stimulate or enhance the division and viability of cells. (cancerquest.org)
  • We have recently characterized a 95 kDa protein, p95, which exhibits enhanced binding to temperature-sensitive p53 (ts-p53) when cells are shifted down to 32.5 degrees C, a temperature at which ts-p53 possesses wild-type (wt)-like activities. (nih.gov)
  • After disease of both P72 and R72 tet-on p53 H1299 cells RelA-silenced cells had been chosen for using puromycin (5 ug/ml) for 14 days and pooled cell lines had been examined for RelA manifestation using western evaluation. (healthweeks.com)
  • After disease of P72 tet-on p53 H1299 cells with CSF1R create or vector control cells had been chosen for using puromycin TAK-733 (5 ug/ml) for 14 days. (healthweeks.com)
  • p53 ChIP-seq data for U2Operating-system cells was from research [28]. (healthweeks.com)
  • Annexin staining was performed using Guava Nexin Reagent (Millipore 4500 For clonogenic success assays tetracycline-inducible p53 H1299 cells expressing vector only (Vector) or CSF1 receptor (CSF1R) had been plated at a denseness of 104 cells in 60-mm tradition meals TAK-733 and incubated over night in regular press (10% FBS 1 P/S in DMEM). (healthweeks.com)
  • Comparison of the chemosensitivity of PANC-1 cells to its wild type p53 transfectants showed that wt-p53 expressing transfectants are more sensitive to both Etoposide and Doxorubucin. (ijbiotech.com)
  • It further showed that neither the PANC1 cells nor its wild type p53 transfectants arrested at G1 in response to X-irradiation. (ijbiotech.com)
  • Southern blot analysis of T-cell receptor genes from parapsoriasis does not identify a dominant clone of T cells. (medscape.com)
  • p53 has been characterized to play a role in blocking the proliferative action of damaged cells and act as an anticancer agent. (thermofisher.com)
  • p53 is found in very low levels in normal cells, however, in a variety of transformed cell lines, it is expressed in high amounts, and believed to contribute to transformation and malignancy. (thermofisher.com)
  • To study oral hyperplastic epithelium, dysplastic epithelium and squamous cell carcinoma todetermine (1) the prevalence of p53 protein immunoreactivity, (2) number of p53 positive cells, and (3) the area of localization of p53 protein immunoreactivity. (bvsalud.org)
  • The localization of these p53 positive cells within the strata (i.e. basal/suprabasal, spinous and superficial layers) of epithelium between 3 groups, and also within each group according to histological grades was recorded. (bvsalud.org)
  • However the quantitative analysis of p53 positive cells and their localization in oral epithelium is of importance as a marker for oral squamous cell carcinoma. (bvsalud.org)
  • This may have an important impact in understanding the biology of wild-type p53 in cancer-transformed cells. (who.int)
  • p53 is a key protein that is altered in all cancer cells. (who.int)
  • A highly expressed protein in tumor cells, encoded by Tpt1 gene. (bvsalud.org)
  • The tumor suppressor protein, p53, is a sequence specific transcription factor that is activated by cellular stress. (thermofisher.com)
  • A report published Physica Energetics calls P53 the "master regulator of cell cycle progression. (breastcancerconqueror.com)
  • p53, mdm-2, p21, and mib-1 expression were not significantly associated with response to chemotherapy, time to progression, or overall survival in the whole patient population or in the docetaxel group. (lu.se)
  • p53 directly regulates JMJD2B gene expression by binding to a canonical p53-consensus motif in the JMJD2B promoter. (escholarship.org)
  • The promoter of p53 induced gene 3 (PIG3) contains a variable amount of tandem repeats (VNTRs) of pentanucleotides (TGYCC)n that's referred to as a p53 binding site. (biotech-angels.com)
  • or more to right now p53 may be the just known molecule that Kobe2602 binds towards the promoter (TGYCC)n [2]. (biotech-angels.com)
  • What's more, the adeno-associated viral vector scientists usually use to deliver a functional DNA sequence can also induce prolonged p53 response. (fiercebiotech.com)
  • METHODS: In a non-randomized pilot trail we tested whether a local therapy based upon an adenoviral gene transfer of wild type p53 in combination with gemcitabine administration would be safe in patients with liver metastases due to pancreatic carcinoma. (omicsdi.org)
  • In 1979, Levine and others discovered the p53 tumor suppressor protein, a molecule that inhibits tumor development. (ias.edu)
  • Retrieved January 224, 2019 from https://neurosciencenews.com/sleep-deprivation-genetics-10638/[/cbtab][cbtab title="Chicago"]Wiley"How Sleep Deprivation Affects Our Genes. (neurosciencenews.com)
  • Now, a team led by scientists in Italy has managed to contain that problem by bypassing the well-known anti-cancer gene p53. (fiercebiotech.com)
  • Inactivation of p53 has been linked to many cancer types, and the gene's cancer-suppressing effect has attracted much interest in the scientific world. (fiercebiotech.com)
  • Although p53 The Gene That Cracked the Cancer Code by Sue Armstrong conveys the details that led up to a great discovery, the read is intense. (sanfranciscobookreview.com)
  • H. pylori seropositivity lost its role in the presence of gastric cancer after multivariate analysis and the presence of p53 and Ki-67 were independent affecting factors for gastric cancer even in an endemic region for H. pylori such as Iran. (scialert.net)
  • This study aims to investigate the association of p53 and D-loop gene with drug resistance and sensitization induced by metformin in ovarian cancer. (oncotarget.com)
  • Now that you have some P53-activating tools at your disposal, there is no need to fear breast cancer! (breastcancerconqueror.com)
  • Survival curves for good prognosis (orange line) and poor prognosis (grey line) breast cancer patients according to 70-gene and 76-gene prognosis profiles are showed ( a and b , respectively). (biomedcentral.com)
  • The larger the gene name, the more frequently that gene is defective in that cancer type. (cancerquest.org)
  • These genes have been found to be either malfunctioning or non-functioning in many different kinds of cancer. (cancerquest.org)
  • As part of this lecture, he will discuss his role with the ACLU in opposing breast cancer gene patents in a case that went to the U.S. Supreme Court. (ias.edu)
  • The HCT116 human being cancer of the colon cell lines (p53+/+ and p53? (biotech-angels.com)
  • Breast cancer risk is influenced by rare coding variants in susceptibility genes, such as BRCA1, and many common, mostly non-coding variants. (cancerindex.org)
  • In breast cancer patients, it is unclear whether measuring p53, mdm-2, or p21 expression provides information on how patients will respond to chemotherapy. (lu.se)
  • 7. Pillay M, Vasudevan DM, Rao CP, Vidya M. p53 expression in oral cancer: observations of a South Indian study. (bvsalud.org)
  • Clinical utility of androgen receptor gene aberrations in circulating cell-free DNA as a biomarker for treatment of castration-resistant prostate cancer. (cdc.gov)
  • Chemotherapy Costs and 21-Gene Recurrence Score Genomic Testing Among Medicare Beneficiaries With Early-Stage Breast Cancer, 2005 to 2011. (cdc.gov)
  • P53-responsive gene 1 is a protein that in humans is encoded by the PRG1 gene. (wikipedia.org)
  • The new research indicates that these modifications are not necessary to activate p53 under conditions of stress or to prevent p53 from throwing a wrench into the cell cycle machinery, when nothing is wrong. (news-medical.net)
  • There is no longer a need for signals to activate these genes. (cancerquest.org)
  • This first category also includes genes that contribute to tumor growth by inhibiting cell death. (cancerquest.org)
  • The normal versions of genes in the first group are called proto-oncogenes. (cancerquest.org)
  • The mutated or otherwise damaged versions of these genes are called oncogenes. (cancerquest.org)
  • We have two copies of each gene and for oncogenes, a single defective copy is enough to cause a cell to divide. (cancerquest.org)
  • Numerous genes have been identified as proto-oncogenes. (cancerquest.org)
  • As stated in the introduction to this section, the defective versions of these genes, known as oncogenes, can cause a cell to divide in an unregulated manner. (cancerquest.org)
  • We also assessed the effect of WSC on the expression of genes involved in cell cycle arrest and inflammation. (who.int)
  • The p53 tumor suppressor protein plays a critical role in orchestrating the genomic response to various stress signals by acting as a master transcriptional regulator. (escholarship.org)
  • By inducing double-stranded breaks (DSBs) at particular genomic sites, they favour the intro of small arbitrary insertions/deletions (indels) through imperfect nonhomologous-end becoming a member of repair, permitting the generation of gene knockouts thereby. (mdm2-inhibitors.com)
  • The p53-response elements inside a genomic series were recognized by slipping a windowpane along the insight series and taking into consideration the spacer in p53 binding sites. (healthweeks.com)
  • Info on p53 ChIP-Seq from doxorubicin-treated lymphoid cell lines can be offered in [27] and reads are in the GEO data source. (healthweeks.com)
  • Overall, we have constructed an atlas of essential and growth-restricting genes in hPSCs, revealing key aspects of cellular essentiality and providing a reference for future studies on human pluripotency. (nature.com)
  • Historians of science can illustrate that neither gene patenting nor basing human classification on race is inevitable: there always have been alternatives. (ias.edu)
  • In the study, the authors dissect a new mechanism driven by cutaneous beta human papillomavirus (HPV) type 38 in altering the function of p53. (who.int)
  • JMJD2B induction attenuates the transcription of key p53 transcriptional targets including p21, PIG3 and PUMA, and this modulation is dependent on the catalytic capacity of JMJD2B. (escholarship.org)
  • With this we could allude to an intrinsic bias of essentiality across cellular compartments, uncover two opposing roles for tumour suppressor genes and link autosomal-recessive disorders with growth-retardation phenotypes to early embryogenesis. (nature.com)
  • Predictive Role of p53 Protein as a Single Marker or Associated to Ki67 Antigen in Oral Carcinogenesis. (bvsalud.org)