Genes whose gain-of-function alterations lead to NEOPLASTIC CELL TRANSFORMATION. They include, for example, genes for activators or stimulators of CELL PROLIFERATION such as growth factors, growth factor receptors, protein kinases, signal transducers, nuclear phosphoproteins, and transcription factors. A prefix of "v-" before oncogene symbols indicates oncogenes captured and transmitted by RETROVIRUSES; the prefix "c-" before the gene symbol of an oncogene indicates it is the cellular homolog (PROTO-ONCOGENES) of a v-oncogene.
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.
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.
Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved in the events that serve to maintain the ordered procession through the cell cycle. Proto-oncogenes have names of the form c-onc.
Family of retrovirus-associated DNA sequences (myc) originally isolated from an avian myelocytomatosis virus. The proto-oncogene myc (c-myc) codes for a nuclear protein which is involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Truncation of the first exon, which appears to regulate c-myc expression, is crucial for tumorigenicity. The human c-myc gene is located at 8q24 on the long arm of chromosome 8.
Products of viral oncogenes, most commonly retroviral oncogenes. They usually have transforming and often protein kinase activities.
ONCOGENE PROTEINS from papillomavirus that deregulate the CELL CYCLE of infected cells and lead to NEOPLASTIC CELL TRANSFORMATION. Papillomavirus E7 proteins have been shown to interact with various regulators of the cell cycle including RETINOBLASTOMA PROTEIN and certain cyclin-dependent kinase inhibitors.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
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 family of transforming proteins isolated from retroviruses such as MOUSE SARCOMA VIRUSES. They are viral-derived members of the raf-kinase family of serine-theonine kinases.
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.
Transforming protein coded by myc oncogenes. The v-myc protein has been found in several replication-defective avian retrovirus isolates which induce a broad spectrum of malignancies.
A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes. It occurs naturally via the excision of a copy of the repeating sequence from the chromosome and its extrachromosomal replication in a plasmid, or via the production of an RNA transcript of the entire repeating sequence of ribosomal RNA followed by the reverse transcription of the molecule to produce an additional copy of the original DNA sequence. Laboratory techniques have been introduced for inducing disproportional replication by unequal crossing over, uptake of DNA from lysed cells, or generation of extrachromosomal sequences from rolling circle replication.
Transforming protein encoded by ras oncogenes. Point mutations in the cellular ras gene (c-ras) can also result in a mutant p21 protein that can transform mammalian cells. Oncogene protein p21(ras) has been directly implicated in human neoplasms, perhaps accounting for as much as 15-20% of all human tumors. This enzyme was formerly listed as EC 3.6.1.47.
Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.
An inheritable change in cells manifested by changes in cell division and growth and alterations in cell surface properties. It is induced by infection with a transforming virus.
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.
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.
Retrovirus-associated DNA sequences (src) originally isolated from the Rous sarcoma virus (RSV). The proto-oncogene src (c-src) codes for a protein that is a member of the tyrosine kinase family and was the first proto-oncogene identified in the human genome. The human c-src gene is located at 20q12-13 on the long arm of chromosome 20.
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.
Proteins coded by oncogenes. They include proteins resulting from the fusion of an oncogene and another gene (ONCOGENE PROTEINS, FUSION).
Family of RNA viruses that infects birds and mammals and encodes the enzyme reverse transcriptase. The family contains seven genera: DELTARETROVIRUS; LENTIVIRUS; RETROVIRUSES TYPE B, MAMMALIAN; ALPHARETROVIRUS; GAMMARETROVIRUS; RETROVIRUSES TYPE D; and SPUMAVIRUS. A key feature of retrovirus biology is the synthesis of a DNA copy of the genome which is integrated into cellular DNA. After integration it is sometimes not expressed but maintained in a latent state (PROVIRUSES).
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.
Established cell cultures that have the potential to propagate indefinitely.
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.
DNA present in neoplastic tissue.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
A cell line derived from cultured tumor cells.
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.
The GENETIC RECOMBINATION of the parts of two or more GENES, including an ONCOGENE as at least one of the fusion partners. Such gene fusions are often detected in neoplastic cells and are transcribed into ONCOGENE FUSION PROTEINS.
Small, monomeric GTP-binding proteins encoded by ras genes (GENES, RAS). The protooncogene-derived protein, PROTO-ONCOGENE PROTEIN P21(RAS), plays a role in normal cellular growth, differentiation and development. The oncogene-derived protein (ONCOGENE PROTEIN P21(RAS)) can play a role in aberrant cellular regulation during neoplastic cell transformation (CELL TRANSFORMATION, NEOPLASTIC). This enzyme was formerly listed as EC 3.6.1.47.
Polyomavirus antigens which cause infection and cellular transformation. The large T antigen is necessary for the initiation of viral DNA synthesis, repression of transcription of the early region and is responsible in conjunction with the middle T antigen for the transformation of primary cells. Small T antigen is necessary for the completion of the productive infection cycle.
Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A family of small, non-enveloped DNA viruses infecting birds and most mammals, especially humans. They are grouped into multiple genera, but the viruses are highly host-species specific and tissue-restricted. They are commonly divided into hundreds of papillomavirus "types", each with specific gene function and gene control regions, despite sequence homology. Human papillomaviruses are found in the genera ALPHAPAPILLOMAVIRUS; BETAPAPILLOMAVIRUS; GAMMAPAPILLOMAVIRUS; and MUPAPILLOMAVIRUS.
Retroviral proteins that have the ability to transform cells. They can induce sarcomas, leukemias, lymphomas, and mammary carcinomas. Not all retroviral proteins are oncogenic.
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 GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular origin.
Retrovirus-associated DNA sequences (abl) originally isolated from the Abelson murine leukemia virus (Ab-MuLV). The proto-oncogene abl (c-abl) codes for a protein that is a member of the tyrosine kinase family. The human c-abl gene is located at 9q34.1 on the long arm of chromosome 9. It is activated by translocation to bcr on chromosome 22 in chronic myelogenous leukemia.
Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.
Widely used technique which exploits the ability of complementary sequences in single-stranded DNAs or RNAs to pair with each other to form a double helix. Hybridization can take place between two complimentary DNA sequences, between a single-stranded DNA and a complementary RNA, or between two RNA sequences. The technique is used to detect and isolate specific sequences, measure homology, or define other characteristics of one or both strands. (Kendrew, Encyclopedia of Molecular Biology, 1994, p503)
Viruses that produce tumors.
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.
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.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
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.
A tyrosine-specific protein kinase encoded by the v-src oncogene of ROUS SARCOMA VIRUS. The transforming activity of pp60(v-src) depends on both the lack of a critical carboxy-terminal tyrosine phosphorylation site at position 527, and the attachment of pp60(v-src) to the plasma membrane which is accomplished by myristylation of its N-terminal glycine.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
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.
Transforming proteins encoded by the abl oncogenes. Oncogenic transformation of c-abl to v-abl occurs by insertional activation that results in deletions of specific N-terminal amino acids.
The number of copies of a given gene present in the cell of an organism. An increase in gene dosage (by GENE DUPLICATION for example) can result in higher levels of gene product formation. GENE DOSAGE COMPENSATION mechanisms result in adjustments to the level GENE EXPRESSION when there are changes or differences in gene dosage.
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.
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.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.
Proteins transcribed from the E1A genome region of ADENOVIRUSES which are involved in positive regulation of transcription of the early genes of host infection.
A type of chromosome aberration characterized by CHROMOSOME BREAKAGE and transfer of the broken-off portion to another location, often to a different chromosome.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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.
RNA present in neoplastic tissue.
Transforming protein coded by jun oncogenes (GENES, JUN). This is a gag-onc fusion protein of about 65 kDa derived from avian sarcoma virus. v-jun lacks a negative regulatory domain that regulates transcription in c-jun.
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.
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.
Transforming proteins coded by fos oncogenes. These proteins have been found in the Finkel-Biskis-Jinkins (FBJ-MSV) and Finkel-Biskis-Reilly (FBR-MSV) murine sarcoma viruses which induce osteogenic sarcomas in mice. The FBJ-MSV v-fos gene encodes a p55-kDa protein and the FBR-MSV v-fos gene encodes a p75-kDa fusion protein.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A raf kinase subclass found at high levels in neuronal tissue. The B-raf Kinases are MAP kinase kinase kinases that have specificity for MAP KINASE KINASE 1 and MAP KINASE KINASE 2.
Abnormal number or structure of chromosomes. Chromosome aberrations may result in CHROMOSOME DISORDERS.
The functional hereditary units of VIRUSES.
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.
A type of ALPHAPAPILLOMAVIRUS especially associated with malignant tumors of the CERVIX and the RESPIRATORY MUCOSA.
Transforming proteins encoded by erbB oncogenes from the avian erythroblastosis virus. The protein is a truncated form of the EGF receptor (RECEPTOR, EPIDERMAL GROWTH FACTOR) whose kinase domain is constitutively activated by deletion of the ligand-binding domain.
A plant genus of the family RUBIACEAE. The root is a source of red dyes (madder color and 1,2,4-trihydroxy-9,10-anthracenedione) and ANTHRAQUINONES.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
A type of IN SITU HYBRIDIZATION in which target sequences are stained with fluorescent dye so their location and size can be determined using fluorescence microscopy. This staining is sufficiently distinct that the hybridization signal can be seen both in metaphase spreads and in interphase nuclei.
Tumors or cancer of the UTERINE CERVIX.
The ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development.
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 replication-defective murine sarcoma virus (SARCOMA VIRUSES, MURINE) capable of transforming mouse lymphoid cells and producing erythroid leukemia after superinfection with murine leukemia viruses (LEUKEMIA VIRUS, MURINE). It has also been found to transform cultured human fibroblasts, rat liver epithelial cells, and rat adrenocortical cells.
Genes whose abnormal expression, or MUTATION are associated with the development, growth, or progression of NEOPLASMS.
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.
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.
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.
A continuous cell line of high contact-inhibition established from NIH Swiss mouse embryo cultures. The cells are useful for DNA transfection and transformation studies. (From ATCC [Internet]. Virginia: American Type Culture Collection; c2002 [cited 2002 Sept 26]. Available from http://www.atcc.org/)
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.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
A leukemia/lymphoma found predominately in children and young adults and characterized LYMPHADENOPATHY and THYMUS GLAND involvement. It most frequently presents as a lymphoma, but a leukemic progression in the bone marrow is common.
The type species of ALPHARETROVIRUS producing latent or manifest lymphoid leukosis in fowl.
Tumors or cancer of the LUNG.
A general term for various neoplastic diseases of the lymphoid tissue.
A ubiquitously expressed raf kinase subclass that plays an important role in SIGNAL TRANSDUCTION. The c-raf Kinases are MAP kinase kinase kinases that have specificity for MAP KINASE KINASE 1 and MAP KINASE KINASE 2.
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 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).
Proteins from the family Retroviridae. The most frequently encountered member of this family is the Rous sarcoma virus protein.
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 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.
Tumors or cancer of the SKIN.
Proteins encoded by adenoviruses that are synthesized prior to, and in the absence of, viral DNA replication. The proteins are involved in both positive and negative regulation of expression in viral and cellular genes, and also affect the stability of viral mRNA. Some are also involved in oncogenic transformation.
A fibroblast growth factor that is expressed primarily during development.
Tumors or cancer of the human BREAST.
Insertion of viral DNA into host-cell DNA. This includes integration of phage DNA into bacterial DNA; (LYSOGENY); to form a PROPHAGE or integration of retroviral DNA into cellular DNA to form a PROVIRUS.
A replication-defective mouse sarcoma virus (SARCOMA VIRUSES, MURINE) first described by J.J. Harvey in 1964.
A genus of the family RETROVIRIDAE with type C morphology, that causes malignant and other diseases in wild birds and domestic fowl.
A method (first developed by E.M. Southern) for detection of DNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Cellular DNA-binding proteins encoded by the c-jun genes (GENES, JUN). They are involved in growth-related transcriptional control. There appear to be three distinct functions: dimerization (with c-fos), DNA-binding, and transcriptional activation. Oncogenic transformation can take place by constitutive expression of c-jun.
Experimental transplantation of neoplasms in laboratory animals for research purposes.
Translation products of a fusion gene derived from CHROMOSOMAL TRANSLOCATION of C-ABL GENES to the genetic locus of the breakpoint cluster region gene on chromosome 22. Several different variants of the bcr-abl fusion proteins occur depending upon the precise location of the chromosomal breakpoint. These variants can be associated with distinct subtypes of leukemias such as PRECURSOR CELL LYMPHOBLASTIC LEUKEMIA-LYMPHOMA; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; and NEUTROPHILIC LEUKEMIA, CHRONIC.
Retrovirus-associated DNA sequences (jun) originally isolated from the avian sarcoma virus 17 (ASV 17). The proto-oncogene jun (c-jun) codes for a nuclear protein which is involved in growth-related transcriptional control. Insertion of c-jun into ASV-17 or the constitutive expression of the c-jun protein produces tumorgenicity. The human c-jun gene is located at 1p31-32 on the short arm of chromosome 1.
Transforming glycoprotein coded by the fms oncogene from the Susan McDonough strain of feline sarcoma virus (SM-FeSV). The oncogene protein v-fms lacks sequences, which, in the highly homologous proto-oncogene protein c-fms (CSF-1 receptor), normally serve to regulate its tyrosine kinase activity. The missing sequences in v-fms mimic the effect of ligand and lead to constitutive cell growth. The protein gp120(v-fms) is post-translationally modified to generate gp140(v-fms).
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.
The transfer of bacterial DNA by phages from an infected bacterium to another bacterium. This also refers to the transfer of genes into eukaryotic cells by viruses. This naturally occurring process is routinely employed as a GENE TRANSFER TECHNIQUE.
A group of replication-defective viruses, in the genus GAMMARETROVIRUS, which are capable of transforming cells, but which replicate and produce tumors only in the presence of Murine leukemia viruses (LEUKEMIA VIRUS, MURINE).
The B-cell leukemia/lymphoma-2 genes, responsible for blocking apoptosis in normal cells, and associated with follicular lymphoma when overexpressed. Overexpression results from the t(14;18) translocation. The human c-bcl-2 gene is located at 18q24 on the long arm of chromosome 18.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
A method for comparing two sets of chromosomal DNA by analyzing differences in the copy number and location of specific sequences. It is used to look for large sequence changes such as deletions, duplications, amplifications, or translocations.
Serine-threonine protein kinases that relay signals from CYTOKINE RECEPTORS and are involved in control of CELL GROWTH PROCESSES; CELL DIFFERENTIATION; and APOPTOSIS.
Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
Receptor protein-tyrosine kinases involved in the signaling of GLIAL CELL-LINE DERIVED NEUROTROPHIC FACTOR ligands. They contain an extracellular cadherin domain and form a receptor complexes with GDNF RECEPTORS. Mutations in ret protein are responsible for HIRSCHSPRUNG DISEASE and MULTIPLE ENDOCRINE NEOPLASIA TYPE 2.
A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)
Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell.
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.
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
A replication-defective strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) capable of transforming lymphoid cells and producing a rapidly progressing lymphoid leukemia after superinfection with FRIEND MURINE LEUKEMIA VIRUS; MOLONEY MURINE LEUKEMIA VIRUS; or RAUSCHER VIRUS.
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.
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.
The erbB-2 gene is a proto-oncogene that codes for the erbB-2 receptor (RECEPTOR, ERBB-2), a protein with structural features similar to the epidermal growth factor receptor. Its name originates from the viral oncogene homolog (v-erbB) which is a truncated form of the chicken erbB gene found in the avian erythroblastosis virus. Overexpression and amplification of the gene is associated with a significant number of adenocarcinomas. The human c-erbB-2 gene is located at 17q21.2.
Genes related to the erbA DNA sequence that was first isolated from the avian erythroblastosis virus (ERYTHROBLASTOSIS VIRUS, AVIAN), v-erbA. In cells, erbA genes encode thyroid hormone receptors (RECEPTORS, THYROID HORMONE). Two distinct c-erbA genes have been identified: erbA-alpha located at 17q21; and erbA-beta located at 3p24. Truncations at the N- and C-terminals of erbA result in products resembling v-erbA. Truncations affect hormone responsiveness but not DNA binding capacity.
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.
Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.
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.
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.
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.
Signal molecules that are involved in the control of cell growth and differentiation.
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)
A cell surface receptor involved in regulation of cell growth and differentiation. It is specific for EPIDERMAL GROWTH FACTOR and EGF-related peptides including TRANSFORMING GROWTH FACTOR ALPHA; AMPHIREGULIN; and HEPARIN-BINDING EGF-LIKE GROWTH FACTOR. The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell.
Aliphatic acids that contain four carbons in a branched-chain configuration. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the 2-carboxypropane structure.
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in leukemia.
Retrovirus-associated DNA sequences (fos) originally isolated from the Finkel-Biskis-Jinkins (FBJ-MSV) and Finkel-Biskis-Reilly (FBR-MSV) murine sarcoma viruses. The proto-oncogene protein c-fos codes for a nuclear protein which is involved in growth-related transcriptional control. The insertion of c-fos into FBJ-MSV or FBR-MSV induces osteogenic sarcomas in mice. The human c-fos gene is located at 14q21-31 on the long arm of chromosome 14.
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.
Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
Common name for the species Gallus gallus, the domestic fowl, in the family Phasianidae, order GALLIFORMES. It is descended from the red jungle fowl of SOUTHEAST ASIA.
Mapping of the KARYOTYPE of a cell.
Myeloid-lymphoid leukemia protein is a transcription factor that maintains high levels of HOMEOTIC GENE expression during development. The GENE for myeloid-lymphoid leukemia protein is commonly disrupted in LEUKEMIA and combines with over 40 partner genes to form FUSION ONCOGENE PROTEINS.
The origin, production or development of cancer through genotypic and phenotypic changes which upset the normal balance between cell proliferation and cell death. Carcinogenesis generally requires a constellation of steps, which may occur quickly or over a period of many years.
Experimentally induced tumors of the LIVER.
A specific pair of GROUP C CHROMOSOMES of the human chromosome classification.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
A class of cellular receptors that have an intrinsic PROTEIN-TYROSINE KINASE activity.
An increased tendency to acquire CHROMOSOME ABERRATIONS when various processes involved in chromosome replication, repair, or segregation are dysfunctional.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Tumors or cancer of the THYMUS GLAND.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The complete genetic complement contained in the DNA of a set of CHROMOSOMES in a HUMAN. The length of the human genome is about 3 billion base pairs.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
Tumors or cancer of the THYROID GLAND.
Biochemical identification of mutational changes in a nucleotide sequence.
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.
A notch receptor that interacts with a variety of ligands and regulates SIGNAL TRANSDUCTION PATHWAYS for multiple cellular processes. It is widely expressed during EMBRYOGENESIS and is essential for EMBRYONIC DEVELOPMENT.
A specific pair of GROUP C CHROMOSOMES of the human chromosome classification.
An essential ribonucleoprotein reverse transcriptase that adds telomeric DNA to the ends of eukaryotic CHROMOSOMES.
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.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
Tumor suppressor genes located on human chromosome 13 in the region 13q14 and coding for a family of phosphoproteins with molecular weights ranging from 104 kDa to 115 kDa. One copy of the wild-type Rb gene is necessary for normal retinal development. Loss or inactivation of both alleles at this locus results in retinoblastoma.
Any method used for determining the location of and relative distances between genes on a chromosome.
Any cell, other than a ZYGOTE, that contains elements (such as NUCLEI and CYTOPLASM) from two or more different cells, usually produced by artificial CELL FUSION.
A cell surface protein-tyrosine kinase receptor that is overexpressed in a variety of ADENOCARCINOMAS. It has extensive homology to and heterodimerizes with the EGF RECEPTOR, the ERBB-3 RECEPTOR, and the ERBB-4 RECEPTOR. Activation of the erbB-2 receptor occurs through heterodimer formation with a ligand-bound erbB receptor family member.
Cellular DNA-binding proteins encoded by the c-fos genes (GENES, FOS). They are involved in growth-related transcriptional control. c-fos combines with c-jun (PROTO-ONCOGENE PROTEINS C-JUN) to form a c-fos/c-jun heterodimer (TRANSCRIPTION FACTOR AP-1) that binds to the TRE (TPA-responsive element) in promoters of certain genes.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
The type species of BETARETROVIRUS commonly latent in mice. It causes mammary adenocarcinoma in a genetically susceptible strain of mice when the appropriate hormonal influences operate.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
Tumors, cancer or other neoplasms produced by exposure to ionizing or non-ionizing radiation.
A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)
Tumors or cancer of the LIVER.
A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (CODON, TERMINATOR). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, TRANSFER) complementary to all codons. These codons are referred to as unassigned codons (CODONS, NONSENSE).
Rats, Inbred F344 are a strain of laboratory rats commonly used in medical research due to their genetic uniformity and susceptibility to various diseases.
Proteins obtained from species of BIRDS.
A malignant epithelial tumor with a glandular organization.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
Species of GAMMARETROVIRUS isolated from fibrosarcoma in cats. The viruses are actually recombinant feline leukemia viruses (FeLV) where part of the genome has been replaced by cellular oncogenes. It is unique to individuals and not transmitted naturally to other cats. FeSVs are replication defective and require FeLV to reproduce.
A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.
A replication-defective murine sarcoma virus (SARCOMA VIRUSES, MURINE) isolated from a rhabdomyosarcoma by Moloney in 1966.
Group of alpharetroviruses (ALPHARETROVIRUS) producing sarcomata and other tumors in chickens and other fowl and also in pigeons, ducks, and RATS.
Ability of neoplasms to infiltrate and actively destroy surrounding tissue.
Change brought about to an organisms genetic composition by unidirectional transfer (TRANSFECTION; TRANSDUCTION, GENETIC; CONJUGATION, GENETIC, etc.) and incorporation of foreign DNA into prokaryotic or eukaryotic cells by recombination of part or all of that DNA into the cell's genome.

Cancer genetics: tumor suppressor meets oncogene. (1/3637)

The adenomatous polyposis coli (APC) tumor suppressor protein is inactivated by mutations in the majority of colorectal cancers. A recent study has revealed that alterations in the APC signaling pathway can result in the transcriptional activation of the c-MYC gene.  (+info)

Diverse developing mouse lineages exhibit high-level c-Myb expression in immature cells and loss of expression upon differentiation. (2/3637)

The c-myb gene encodes a sequence specific transactivator that is required for fetal hematopoiesis, but its potential role in other tissues is less clear because of the early fetal demise of mice with targeted deletions of the c-myb gene and incomplete of knowledge about c-myb's expression pattern. In the hematopoietic system, c-Myb protein acts on target genes whose expression is restricted to individual lineages, despite Myb's presence and role in multiple immature lineages. This suggests that c-Myb actions within different cell type-specific contexts are strongly affected by combinatorial interactions. To consider the possibility of similar c-Myb actions could extend into non-hematopoietic systems in other cell and tissue compartments, we characterized c-myb expression in developing and adult mice using in situ hybridization and correlated this with stage-specific differentiation and mitotic activity. Diverse tissues exhibited strong c-myb expression during development, notably tooth buds, the thyroid primordium, developing trachea and proximal branching airway epithelium, hair follicles, hematopoietic cells, and gastrointestinal crypt epithelial cells. The latter three of these all maintained high expression into adulthood, but with characteristic restriction to immature cell lineages prior to their terminal differentiation. In all sites, during fetal and adult stages, loss of c-Myb expression correlated strikingly with the initiation of terminal differentiation, but not the loss of mitotic activity. Based on these data, we hypothesize that c-Myb's function during cellular differentiation is both an activator of immature gene expression and a suppressor of terminal differentiation in diverse lineages.  (+info)

Insertion of excised IgH switch sequences causes overexpression of cyclin D1 in a myeloma tumor cell. (3/3637)

Oncogenes are often dysregulated in B cell tumors as a result of a reciprocal translocation involving an immunoglobulin locus. The translocations are caused by errors in two developmentally regulated DNA recombination processes: V(D)J and IgH switch recombination. Both processes share the property of joining discontinuous sequences from one chromosome and releasing intervening sequences as circles that are lost from progeny cells. Here we show that these intervening sequences may instead insert in the genome and that during productive IgH mu-epsilon switch recombination in U266 myeloma tumor cells, a portion of the excised IgH switch intervening sequences containing the 3' alpha-1 enhancer has inserted on chromosome 11q13, resulting in overexpression of the adjacent cyclin D1 oncogene.  (+info)

Molecular mechanisms of proliferation in endometrial tumour cells. (4/3637)

The human endometrium normally undergoes a cyclic proliferation process followed by differentiation under the influence of ovarian steroids and locally produced growth and differentiation factors. Understanding of the molecular mechanisms involved in controlling these processes is of great interest, since imbalances between proliferation- and differentiation-promoting signals can have pathophysiological consequences ranging from infertility to endometrial hyperplasia and tumour formation. The present work reviews aspects of the role played by oncogenes and ovarian steroid receptors in modulating proliferation of endometrial tumour cells. The expression pattern and possible roles of protein kinase C (PKC) subunits are discussed in the context of response-specificity of endometrial tumour cells to tumour-promoting agents such as 12-O-tetradecanoyl-phorbol acetate (TPA) and possible implications for anti-tumour therapy.  (+info)

Molecular detection of tumor cells in bronchoalveolar lavage fluid from patients with early stage lung cancer. (5/3637)

BACKGROUND: Conventional cytologic analysis of sputum is an insensitive test for the diagnosis of non-small-cell lung cancer (NSCLC). We have recently demonstrated that polymerase chain reaction (PCR)-based molecular methods are more sensitive than cytologic analysis in diagnosing bladder cancer. In this study, we examined whether molecular assays could identify cancer cells in bronchoalveolar lavage (BAL) fluid. METHODS: Tumor-specific oncogene mutations, CpG-island methylation status, and microsatellite alterations in the DNA of cells in BAL fluid from 50 consecutive patients with resectable (stages I through IIIa) NSCLC were assessed by use of four PCR-based techniques. RESULTS: Of 50 tumors, 28 contained a p53 mutation, and the identical mutation was detected with a plaque hybridization assay in the BAL fluid of 39% (11 of 28) of the corresponding patients. Eight of 19 adenocarcinomas contained a K-ras mutation, and the identical mutation was detected with a mutation ligation assay in the BAL fluid of 50% (four of eight) of the corresponding patients. The p16 gene was methylated in 19 of 50 tumors, and methylated p16 alleles were detected in the BAL fluid of 63% (12 of 19) of the corresponding patients. Microsatellite instability in at least one marker was detected with a panel of 15 markers frequently altered in NSCLC in 23 of 50 tumors; the identical alteration was detected in the BAL fluid of 14% (three of 22) of the corresponding patients. When all four techniques were used, mutations or microsatellite instability was detected in the paired BAL fluid of 23 (53%) of the 43 patients with tumors carrying a genetic alteration. CONCLUSION: Although still limited by sensitivity, molecular diagnostic strategies can detect the presence of neoplastic cells in the proximal airway of patients with surgically resectable NSCLC.  (+info)

Search for oncogenic regulators in an autocrine tumor model using differential display PCR: identification of novel candidate genes including the calcium channel mtrp6. (6/3637)

A hemopoietic multistep tumor model, in which IL-3 dependent PB-3c mast cells, following expression of v-H-ras progress in vivo to IL-3 producing autocrine tumors has previously been established. Central for this oncogenic progression is a recessive step, which is reversible by cell fusion and leads to stabilization of IL-3 mRNA with concomitant activation of the autocrine loop. Comparing the IL-3 dependent PB-3c and the IL-3 autocrine V2D1 tumor cells with differential display PCR revealed 12 differentially expressed genes of which eight were upregulated and four downregulated in the tumor. They included four proteases (mouse mast cell protease 2, granzyme B, pepsinogen F and serine protease 1) and two metabolic enzymes (adenine phosphoribosyltransferase and fructose1,6-bisphosphatase). For validation, expression of the identified genes was tested in independent PB-3c precursor clones and their tumor derivatives. Expression of an endogenous retroviral IAP element and three unknown transcripts were consistently upregulated in all tumor lines. In somatic cell hybrids, two of these unknown cDNAs showed a dominant and one a recessive expression pattern. One transcript, expressed in the precursor but downregulated in the tumor cells, was cloned and identified as the murine calcium channel mtrp6.  (+info)

Induction of apoptosis by N-(4-hydroxyphenyl)retinamide and its association with reactive oxygen species, nuclear retinoic acid receptors, and apoptosis-related genes in human prostate carcinoma cells. (7/3637)

The synthetic retinoid N-(4-hydroxyphenyl)retinamide (4HPR) has been shown to induce apoptosis in various malignant cells including human prostate carcinoma cells (HPC). We examined several possible mechanisms by which 4HPR could induce apoptosis in HPC cells. 4HPR exhibited concentration- and time-dependent decrease in cell number both in androgen-dependent (LNCaP) and -independent (DU145 and PC-3) cells. The 4HPR concentrations causing 50% decrease in cell number in LNCaP, DU145, and PC-3 cultures were 0.9 +/- 0.16, 4.4 +/- 0.45, and 3.0 +/- 1.0 microM, respectively, indicating that LNCaP cells were more sensitive to 4HPR than the other cells. 4HPR-induced apoptosis in all three cell lines was evidenced by increased enzymatic labeling of DNA breaks and formation of a DNA ladder. 4HPR increased the level of reactive oxygen species, especially in LNCaP cells. 4HPR-induced apoptosis could be suppressed in LNCaP cells by antioxidant and in DU145 cells by a nuclear retinoic acid receptor-specific antagonist, suggesting the involvement of reactive oxygen species or retinoic acid receptors in mediating apoptosis induced by 4HPR in the different HPC cells. Furthermore, 4HPR modulated the expression levels of some apoptosis-related gene (p21, c-myc, and c-jun), which may also contribute to the induction of apoptosis by 4HPR in HPC cells.  (+info)

An ankyrin-like protein with transmembrane domains is specifically lost after oncogenic transformation of human fibroblasts. (8/3637)

We have identified a novel transformation-sensitive mRNA, which is present in cultured fibroblasts but is lacking in SV40 transformed cells as well as in many mesenchymal tumor cell lines. The corresponding gene is located on human chromosome 8 in band 8q13. The open reading frame of the mRNA encodes a protein of 1119 amino acids forming two distinct domains. The N-terminal domain consists of 18 repeats that are related to the cytoskeletal protein ankyrin. The C-terminal domain contains six putative transmembrane segments that resemble many ion channels. This overall structure is reminiscent of TRP-like proteins that function as store-operated calcium channels. The novel protein with an Mr of 130 kDa is expressed at a very low level in human fibroblasts and at a moderate level in liposarcoma cells. Overexpression in eukaryotic cells appears to interfere with normal growth, suggesting that it might play a direct or indirect role in signal transduction and growth control.  (+info)

Cell transformation, neoplastic refers to the process by which normal cells in the body undergo genetic changes that cause them to become cancerous or malignant. This process involves the accumulation of mutations in genes that regulate cell growth, division, and death, leading to uncontrolled cell proliferation and the formation of tumors. Neoplastic transformation can occur in any type of cell in the body, and it can be caused by a variety of factors, including exposure to carcinogens, radiation, viruses, and inherited genetic mutations. Once a cell has undergone neoplastic transformation, it can continue to divide and grow uncontrollably, invading nearby tissues and spreading to other parts of the body through the bloodstream or lymphatic system. The diagnosis of neoplastic transformation typically involves a combination of clinical examination, imaging studies, and biopsy. Treatment options for neoplastic transformation depend on the type and stage of cancer, as well as the patient's overall health and preferences. Common treatments include surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy.

Oncogene proteins, viral, are proteins that are encoded by viruses and have the potential to cause cancer in infected cells. These proteins can interfere with the normal functioning of cellular genes and signaling pathways, leading to uncontrolled cell growth and division. Examples of viral oncogenes include the E6 and E7 proteins of human papillomavirus (HPV), which are associated with cervical cancer, and the v-Abl protein of the Philadelphia chromosome, which is associated with chronic myelogenous leukemia. The study of viral oncogenes is an important area of research in cancer biology and the development of new cancer treatments.

Papillomavirus E7 proteins are a group of proteins that are encoded by human papillomaviruses (HPVs). These proteins play a critical role in the pathogenesis of HPV-related diseases, particularly cervical cancer. The E7 protein is expressed in the nucleus of infected cells and binds to and inactivates a tumor suppressor protein called pRb (retinoblastoma protein). This inactivation leads to the release of other transcription factors that promote cell proliferation and survival, ultimately contributing to the development of precancerous lesions and cancer. E7 proteins have also been shown to interact with other cellular proteins, including cdk4, cdk6, and cyclin D1, which are involved in cell cycle regulation and can contribute to the development of cancer. Overall, the E7 protein is a key factor in the pathogenesis of HPV-related diseases and is a target for the development of new therapies for these conditions.

Proto-oncogene proteins c-myc is a family of proteins that play a role in regulating cell growth and division. They are also known as myc proteins. The c-myc protein is encoded by the MYC gene, which is located on chromosome 8. The c-myc protein is a transcription factor, which means that it helps to regulate the expression of other genes. When the c-myc protein is overexpressed or mutated, it can contribute to the development of cancer. In normal cells, the c-myc protein helps to control the cell cycle and prevent uncontrolled cell growth. However, in cancer cells, the c-myc protein may be overactive or mutated, leading to uncontrolled cell growth and the formation of tumors.

Oncogene proteins v-raf are a type of protein that are involved in the development of cancer. They are a sub-type of the larger family of proteins called ras oncogenes, which are found in many different types of cells and play a role in regulating cell growth and division. The v-raf oncogene is specifically associated with the development of certain types of cancer, such as leukemia and certain types of solid tumors. When the v-raf oncogene is mutated or overexpressed, it can cause uncontrolled cell growth and division, leading to the development of cancer.

A cell line, transformed, is a type of cell that has been genetically altered to become cancerous or immortal. This is typically done through exposure to chemicals, radiation, or viruses that cause changes in the DNA of the cell, allowing it to grow and divide uncontrollably. Transformed cell lines are often used in research to study cancer biology and develop new treatments, as they can be easily grown and manipulated in the laboratory. They are also used in the production of vaccines and other medical products.

Cell transformation by viruses refers to the process by which viruses alter the normal functioning of host cells, leading to uncontrolled cell growth and division. This can result in the development of cancerous tumors. Viruses can cause cell transformation by introducing genetic material into the host cell, which can disrupt normal cellular processes and lead to the activation of oncogenes (genes that promote cell growth) or the inactivation of tumor suppressor genes (genes that prevent uncontrolled cell growth). There are several types of viruses that can cause cell transformation, including retroviruses (such as HIV), oncoviruses (such as hepatitis B and C viruses), and papillomaviruses (such as the human papillomavirus, which can cause cervical cancer). Cell transformation by viruses is an important area of research in the field of cancer biology, as it helps to identify the molecular mechanisms underlying cancer development and can lead to the development of new treatments for cancer.

In the medical field, neoplasms refer to abnormal growths or tumors of cells that can occur in any part of the body. These growths can be either benign (non-cancerous) or malignant (cancerous). Benign neoplasms are usually slow-growing and do not spread to other parts of the body. They can cause symptoms such as pain, swelling, or difficulty moving the affected area. Examples of benign neoplasms include lipomas (fatty tumors), hemangiomas (vascular tumors), and fibromas (fibrous tumors). Malignant neoplasms, on the other hand, are cancerous and can spread to other parts of the body through the bloodstream or lymphatic system. They can cause a wide range of symptoms, depending on the location and stage of the cancer. Examples of malignant neoplasms include carcinomas (cancers that start in epithelial cells), sarcomas (cancers that start in connective tissue), and leukemias (cancers that start in blood cells). The diagnosis of neoplasms typically involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy (the removal of a small sample of tissue for examination under a microscope). Treatment options for neoplasms depend on the type, stage, and location of the cancer, as well as the patient's overall health and preferences.

Proto-oncogenes are normal genes that are involved in regulating cell growth and division. When these genes are mutated or overexpressed, they can become oncogenes, which can lead to the development of cancer. Proto-oncogenes are also known as proto-oncogene proteins.

Oncogenes are genes that have the potential to cause cancer when they are mutated or expressed at high levels. Oncogenes are also known as proto-oncogenes, and they are involved in regulating cell growth and division. When oncogenes are mutated or expressed at high levels, they can cause uncontrolled cell growth and division, leading to the development of cancer. Oncogene proteins are the proteins that are produced by oncogenes. These proteins can play a variety of roles in the development and progression of cancer, including promoting cell growth and division, inhibiting cell death, and contributing to the formation of tumors.

In the medical field, a cell line refers to a group of cells that have been derived from a single parent cell and have the ability to divide and grow indefinitely in culture. These cells are typically grown in a laboratory setting and are used for research purposes, such as studying the effects of drugs or investigating the underlying mechanisms of diseases. Cell lines are often derived from cancerous cells, as these cells tend to divide and grow more rapidly than normal cells. However, they can also be derived from normal cells, such as fibroblasts or epithelial cells. Cell lines are characterized by their unique genetic makeup, which can be used to identify them and compare them to other cell lines. Because cell lines can be grown in large quantities and are relatively easy to maintain, they are a valuable tool in medical research. They allow researchers to study the effects of drugs and other treatments on specific cell types, and to investigate the underlying mechanisms of diseases at the cellular level.

DNA, or deoxyribonucleic acid, is a molecule that carries genetic information in living organisms. It is composed of four types of nitrogen-containing molecules called nucleotides, which are arranged in a specific sequence to form the genetic code. Neoplasm refers to an abnormal growth of cells in the body, which can be either benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can be caused by a variety of factors, including genetic mutations, exposure to carcinogens, and hormonal imbalances. In the medical field, DNA and neoplasms are closely related because many types of cancer are caused by mutations in the DNA of cells. These mutations can lead to uncontrolled cell growth and the formation of tumors. DNA analysis is often used to diagnose and treat cancer, as well as to identify individuals who are at increased risk of developing the disease.

Cell division is the process by which a single cell divides into two or more daughter cells. This process is essential for the growth, development, and repair of tissues in the body. There are two main types of cell division: mitosis and meiosis. Mitosis is the process by which somatic cells (non-reproductive cells) divide to produce two identical daughter cells with the same number of chromosomes as the parent cell. This process is essential for the growth and repair of tissues in the body. Meiosis, on the other hand, is the process by which germ cells (reproductive cells) divide to produce four genetically diverse daughter cells with half the number of chromosomes as the parent cell. This process is essential for sexual reproduction. Abnormalities in cell division can lead to a variety of medical conditions, including cancer. In cancer, cells divide uncontrollably and form tumors, which can invade nearby tissues and spread to other parts of the body.

In the medical field, a base sequence refers to the specific order of nucleotides (adenine, thymine, cytosine, and guanine) that make up the genetic material (DNA or RNA) of an organism. The base sequence determines the genetic information encoded within the DNA molecule and ultimately determines the traits and characteristics of an individual. The base sequence can be analyzed using various techniques, such as DNA sequencing, to identify genetic variations or mutations that may be associated with certain diseases or conditions.

Tumor suppressor protein p53 is a protein that plays a crucial role in regulating cell growth and preventing the development of cancer. It is encoded by the TP53 gene and is one of the most commonly mutated genes in human cancer. The p53 protein acts as a "guardian of the genome" by detecting DNA damage and initiating a series of cellular responses to repair the damage or trigger programmed cell death (apoptosis) if the damage is too severe. This helps to prevent the accumulation of mutations in the DNA that can lead to the development of cancer. In addition to its role in preventing cancer, p53 also plays a role in regulating cell cycle progression, DNA repair, and the response to cellular stress. Mutations in the TP53 gene can lead to the production of a non-functional or mutated p53 protein, which can result in the loss of these important functions and contribute to the development of cancer. Overall, the p53 protein is a critical regulator of cell growth and survival, and its dysfunction is a common feature of many types of cancer.

3T3 cells are a type of mouse fibroblast cell line that are commonly used in biomedical research. They are derived from the mouse embryo and are known for their ability to grow and divide indefinitely in culture. 3T3 cells are often used as a model system for studying cell growth, differentiation, and other cellular processes. They are also used in the development of new drugs and therapies, as well as in the testing of cosmetic and other products for safety and efficacy.

A cell line, tumor is a type of cell culture that is derived from a cancerous tumor. These cell lines are grown in a laboratory setting and are used for research purposes, such as studying the biology of cancer and testing potential new treatments. They are typically immortalized, meaning that they can continue to divide and grow indefinitely, and they often exhibit the characteristics of the original tumor from which they were derived, such as specific genetic mutations or protein expression patterns. Cell lines, tumor are an important tool in cancer research and have been used to develop many of the treatments that are currently available for cancer patients.

Ras proteins are a family of small, membrane-bound GTPases that play a critical role in regulating cell growth and division. They are involved in transmitting signals from cell surface receptors to the cell interior, where they activate a cascade of downstream signaling pathways that ultimately control cell behavior. Ras proteins are found in all eukaryotic cells and are encoded by three genes: HRAS, KRAS, and NRAS. These genes are frequently mutated in many types of cancer, leading to the production of constitutively active Ras proteins that are always "on" and promote uncontrolled cell growth and division. In the medical field, Ras proteins are an important target for cancer therapy, as drugs that can inhibit the activity of Ras proteins have the potential to slow or stop the growth of cancer cells. However, developing effective Ras inhibitors has proven to be a challenging task, as Ras proteins are highly conserved and essential for normal cell function. Nonetheless, ongoing research continues to explore new ways to target Ras proteins in cancer treatment.

Antigens, Polyomavirus Transforming are proteins that are produced by certain types of polyomaviruses, which are a group of viruses that can cause cancer in humans and animals. These antigens are produced by the virus after it infects a cell and transforms it into a cancerous cell. The antigens are recognized by the immune system as foreign and can trigger an immune response, which can help to control the growth and spread of the cancerous cells. However, in some cases, the immune system may not be able to effectively recognize and attack the cancerous cells, which can lead to the progression of the cancer.

MicroRNAs (miRNAs) are small, non-coding RNA molecules that play a crucial role in regulating gene expression at the post-transcriptional level. They are typically 18-24 nucleotides in length and are transcribed from endogenous genes. In the medical field, miRNAs have been found to be involved in a wide range of biological processes, including cell growth, differentiation, apoptosis, and metabolism. Dysregulation of miRNA expression has been implicated in various diseases, including cancer, cardiovascular disease, neurological disorders, and infectious diseases. MiRNAs can act as either oncogenes or tumor suppressors, depending on the target gene they regulate. They can also be used as diagnostic and prognostic markers for various diseases, as well as therapeutic targets for the development of new drugs.

Retroviridae Proteins, Oncogenic refers to proteins encoded by retroviruses that have the ability to cause cancer in infected cells. Retroviruses are a type of virus that use RNA as their genetic material and reverse transcribe their RNA genome into DNA, which is then integrated into the host cell's genome. Oncogenic retroviruses can cause cancer by inserting their DNA into the host cell's genome at a specific location, called a viral integration site, which can disrupt the normal functioning of cellular genes and lead to uncontrolled cell growth and division. Examples of oncogenic retroviruses include the human immunodeficiency virus (HIV) and the avian leukosis virus (ALV).

In the medical field, RNA, Messenger (mRNA) refers to a type of RNA molecule that carries genetic information from DNA in the nucleus of a cell to the ribosomes, where proteins are synthesized. During the process of transcription, the DNA sequence of a gene is copied into a complementary RNA sequence called messenger RNA (mRNA). This mRNA molecule then leaves the nucleus and travels to the cytoplasm of the cell, where it binds to ribosomes and serves as a template for the synthesis of a specific protein. The sequence of nucleotides in the mRNA molecule determines the sequence of amino acids in the protein that is synthesized. Therefore, changes in the sequence of nucleotides in the mRNA molecule can result in changes in the amino acid sequence of the protein, which can affect the function of the protein and potentially lead to disease. mRNA molecules are often used in medical research and therapy as a way to introduce new genetic information into cells. For example, mRNA vaccines work by introducing a small piece of mRNA that encodes for a specific protein, which triggers an immune response in the body.

Oncogene proteins, fusion refers to the abnormal combination of two or more genes that results in the production of a new protein that is not normally present in the body. These fusion proteins are often associated with the development of cancer, as they can disrupt normal cellular processes and lead to uncontrolled cell growth and division. Fusion proteins can occur as a result of genetic mutations or chromosomal rearrangements, such as translocations or inversions. They can be detected through various diagnostic tests, including molecular genetic testing and immunohistochemistry. Examples of oncogene proteins, fusion include BCR-ABL1 in chronic myeloid leukemia, EML4-ALK in non-small cell lung cancer, and NPM-ALK in anaplastic large cell lymphoma. Targeted therapies that specifically inhibit the activity of these fusion proteins are often used in the treatment of these cancers.

Protein-tyrosine kinases (PTKs) are a family of enzymes that play a crucial role in various cellular processes, including cell growth, differentiation, metabolism, and signal transduction. These enzymes catalyze the transfer of a phosphate group from ATP to the hydroxyl group of tyrosine residues on specific target proteins, thereby modifying their activity, localization, or interactions with other molecules. PTKs are involved in many diseases, including cancer, cardiovascular disease, and neurological disorders. They are also targets for many drugs, including those used to treat cancer and other diseases. In the medical field, PTKs are studied to understand their role in disease pathogenesis and to develop new therapeutic strategies.

Repressor proteins are a class of proteins that regulate gene expression by binding to specific DNA sequences and preventing the transcription of the associated gene. They are often involved in controlling the expression of genes that are involved in cellular processes such as metabolism, growth, and differentiation. Repressor proteins can be classified into two main types: transcriptional repressors and post-transcriptional repressors. Transcriptional repressors bind to specific DNA sequences near the promoter region of a gene, which prevents the binding of RNA polymerase and other transcription factors, thereby inhibiting the transcription of the gene. Post-transcriptional repressors, on the other hand, bind to the mRNA of a gene, which prevents its translation into protein or causes its degradation, thereby reducing the amount of protein produced. Repressor proteins play important roles in many biological processes, including development, differentiation, and cellular response to environmental stimuli. They are also involved in the regulation of many diseases, including cancer, neurological disorders, and metabolic disorders.

Oncogene proteins v-abl are a type of protein that are involved in the development of cancer. They are also known as tyrosine kinases, which means they have the ability to add phosphate groups to tyrosine residues on other proteins. This process can activate the proteins and lead to uncontrolled cell growth and division, which can result in the formation of tumors. v-abl proteins are found in a variety of cancers, including leukemia, lymphoma, and sarcoma. They are also involved in the development of certain solid tumors, such as breast cancer and prostate cancer. Treatment for cancers that are caused by v-abl proteins may include targeted therapies that specifically inhibit the activity of these proteins.

Apoptosis is a programmed cell death process that occurs naturally in the body. It is a vital mechanism for maintaining tissue homeostasis and eliminating damaged or unwanted cells. During apoptosis, cells undergo a series of changes that ultimately lead to their death and removal from the body. These changes include chromatin condensation, DNA fragmentation, and the formation of apoptotic bodies, which are engulfed by neighboring cells or removed by immune cells. Apoptosis plays a critical role in many physiological processes, including embryonic development, tissue repair, and immune function. However, when apoptosis is disrupted or dysregulated, it can contribute to the development of various diseases, including cancer, autoimmune disorders, and neurodegenerative diseases.

DNA-binding proteins are a class of proteins that interact with DNA molecules to regulate gene expression. These proteins recognize specific DNA sequences and bind to them, thereby affecting the transcription of genes into messenger RNA (mRNA) and ultimately the production of proteins. DNA-binding proteins play a crucial role in many biological processes, including cell division, differentiation, and development. They can act as activators or repressors of gene expression, depending on the specific DNA sequence they bind to and the cellular context in which they are expressed. Examples of DNA-binding proteins include transcription factors, histones, and non-histone chromosomal proteins. Transcription factors are proteins that bind to specific DNA sequences and regulate the transcription of genes by recruiting RNA polymerase and other factors to the promoter region of a gene. Histones are proteins that package DNA into chromatin, and non-histone chromosomal proteins help to organize and regulate chromatin structure. DNA-binding proteins are important targets for drug discovery and development, as they play a central role in many diseases, including cancer, genetic disorders, and infectious diseases.

Transcription factors are proteins that regulate gene expression by binding to specific DNA sequences and controlling the transcription of genetic information from DNA to RNA. They play a crucial role in the development and function of cells and tissues in the body. In the medical field, transcription factors are often studied as potential targets for the treatment of diseases such as cancer, where their activity is often dysregulated. For example, some transcription factors are overexpressed in certain types of cancer cells, and inhibiting their activity may help to slow or stop the growth of these cells. Transcription factors are also important in the development of stem cells, which have the ability to differentiate into a wide variety of cell types. By understanding how transcription factors regulate gene expression in stem cells, researchers may be able to develop new therapies for diseases such as diabetes and heart disease. Overall, transcription factors are a critical component of gene regulation and have important implications for the development and treatment of many diseases.

Cell proliferation refers to the process of cell division and growth, which is essential for the maintenance and repair of tissues in the body. In the medical field, cell proliferation is often studied in the context of cancer, where uncontrolled cell proliferation can lead to the formation of tumors and the spread of cancer cells to other parts of the body. In normal cells, cell proliferation is tightly regulated by a complex network of signaling pathways and feedback mechanisms that ensure that cells divide only when necessary and that they stop dividing when they have reached their full capacity. However, in cancer cells, these regulatory mechanisms can become disrupted, leading to uncontrolled cell proliferation and the formation of tumors. In addition to cancer, cell proliferation is also important in other medical conditions, such as wound healing, tissue regeneration, and the development of embryos. Understanding the mechanisms that regulate cell proliferation is therefore critical for developing new treatments for cancer and other diseases.

Adenovirus E1A proteins are a group of proteins encoded by the E1A gene of adenoviruses. These proteins play a crucial role in the viral life cycle and are involved in the transformation of host cells. The E1A proteins interact with various cellular proteins and modulate their activities, leading to the deregulation of cell growth and division. This can result in the uncontrolled proliferation of cells, which is a hallmark of cancer. Therefore, the study of E1A proteins has important implications for understanding the pathogenesis of adenovirus infections and the development of cancer.

Translocation, genetic refers to a type of chromosomal rearrangement in which a segment of one chromosome breaks off and attaches to a different chromosome or to a different part of the same chromosome. This can result in a variety of genetic disorders, depending on the specific genes that are affected by the translocation. Some examples of genetic disorders that can be caused by translocations include leukemia, lymphoma, and certain types of congenital heart defects. Translocations can be detected through genetic testing, such as karyotyping, and can be important for diagnosing and treating genetic disorders.

In the medical field, "Cells, Cultured" refers to cells that have been grown and maintained in a controlled environment outside of their natural biological context, typically in a laboratory setting. This process is known as cell culture and involves the isolation of cells from a tissue or organism, followed by their growth and proliferation in a nutrient-rich medium. Cultured cells can be derived from a variety of sources, including human or animal tissues, and can be used for a wide range of applications in medicine and research. For example, cultured cells can be used to study the behavior and function of specific cell types, to develop new drugs and therapies, and to test the safety and efficacy of medical products. Cultured cells can be grown in various types of containers, such as flasks or Petri dishes, and can be maintained at different temperatures and humidity levels to optimize their growth and survival. The medium used to culture cells typically contains a combination of nutrients, growth factors, and other substances that support cell growth and proliferation. Overall, the use of cultured cells has revolutionized medical research and has led to many important discoveries and advancements in the field of medicine.

RNA, Neoplasm refers to the presence of abnormal RNA molecules in a neoplasm, which is a mass of abnormal cells that grow uncontrollably in the body. RNA is a type of genetic material that plays a crucial role in the regulation of gene expression and protein synthesis. In neoplasms, abnormal RNA molecules can be produced due to mutations in the DNA that codes for RNA. These abnormal RNA molecules can affect the normal functioning of cells and contribute to the development and progression of cancer. The detection and analysis of RNA in neoplasms can provide important information about the genetic changes that are occurring in the cells and can help guide the development of targeted therapies for cancer treatment.

Cell aging, also known as cellular senescence, is a natural process that occurs as cells divide and replicate over time. As cells age, they become less efficient at carrying out their normal functions and may accumulate damage to their DNA, proteins, and other cellular components. This damage can lead to a decline in the overall health and function of the cell, and can contribute to the development of age-related diseases and conditions. In the medical field, cell aging is an important area of research, as it is closely linked to the aging process itself and to many age-related diseases, such as cancer, cardiovascular disease, and neurodegenerative disorders. Researchers are studying the mechanisms of cell aging in order to develop new treatments and therapies to slow down or reverse the aging process, and to prevent or treat age-related diseases.

Oncogene proteins v-fos are a type of protein that are involved in the development of cancer. They are encoded by the v-fos gene, which is a member of the fos oncogene family. The v-fos protein is a transcription factor that regulates the expression of other genes, and it plays a role in cell proliferation, differentiation, and survival. When the v-fos gene is mutated or overexpressed, it can lead to the uncontrolled growth and division of cells, which can result in the development of cancer.

Proto-oncogene proteins B-raf, also known as B-Raf or Raf-1, are a family of serine/threonine protein kinases that play a critical role in regulating cell growth and division. They are encoded by the B-raf gene and are found in a variety of tissues throughout the body. B-Raf is a member of the Raf family of kinases, which are involved in the Ras signaling pathway. This pathway is a key regulator of cell proliferation, differentiation, and survival, and is often dysregulated in cancer. B-Raf is activated by phosphorylation, which leads to the activation of downstream signaling molecules and the promotion of cell growth and division. Mutations in the B-raf gene are associated with several types of cancer, including melanoma, colorectal cancer, and thyroid cancer. These mutations can lead to the constitutive activation of the B-Raf protein, which can promote uncontrolled cell growth and division, leading to the development of cancer. In the medical field, B-Raf inhibitors are used as targeted therapies for the treatment of certain types of cancer, particularly melanoma. These drugs work by inhibiting the activity of the B-Raf protein, thereby blocking the Ras signaling pathway and preventing the promotion of cell growth and division.

Chromosome aberrations refer to changes or abnormalities in the structure or number of chromosomes in a cell. These changes can occur naturally during cell division or as a result of exposure to mutagens such as radiation or certain chemicals. Chromosome aberrations can be classified into several types, including deletions, duplications, inversions, translocations, and aneuploidy. These changes can have significant effects on the function of the affected cells and can lead to a variety of medical conditions, including cancer, genetic disorders, and birth defects. In the medical field, chromosome aberrations are often studied as a way to understand the genetic basis of disease and to develop new treatments.

Neoplasm proteins are proteins that are produced by cancer cells. These proteins are often abnormal and can contribute to the growth and spread of cancer. They can be detected in the blood or other body fluids, and their presence can be used as a diagnostic tool for cancer. Some neoplasm proteins are also being studied as potential targets for cancer treatment.

Oncogene proteins v-erbB are a type of protein that are involved in the development of cancer. They are also known as receptor tyrosine kinases (RTKs) and are activated when they bind to specific growth factors. When v-erbB proteins are overactive or mutated, they can cause uncontrolled cell growth and division, leading to the formation of tumors. v-erbB proteins are found in a variety of cancers, including breast cancer, lung cancer, and leukemia. They are also being studied as potential targets for cancer treatment.

In the medical field, "Neoplasms, Experimental" refers to the study of neoplasms (abnormal growths of cells) in experimental settings, such as in laboratory animals or in vitro cell cultures. These studies are typically conducted to better understand the underlying mechanisms of neoplasms and to develop new treatments for cancer and other types of neoplastic diseases. Experimental neoplasms may be induced by various factors, including genetic mutations, exposure to carcinogens, or other forms of cellular stress. The results of these studies can provide valuable insights into the biology of neoplasms and help to identify potential targets for therapeutic intervention.

Uterine cervical neoplasms refer to abnormal growths or tumors that develop in the cervix, which is the lower part of the uterus that connects to the vagina. These neoplasms can be either benign (non-cancerous) or malignant (cancerous). Cervical neoplasms can be classified into different types based on their characteristics and degree of malignancy. The most common type of cervical neoplasm is cervical intraepithelial neoplasia (CIN), which is a precancerous condition that can progress to invasive cervical cancer if left untreated. Cervical cancer is a serious health concern worldwide, and it is the fourth most common cancer in women globally. However, with regular screening and appropriate treatment, the prognosis for cervical cancer is generally good when it is detected early.

Tumor suppressor proteins are a group of proteins that play a crucial role in regulating cell growth and preventing the development of cancer. These proteins act as brakes on the cell cycle, preventing cells from dividing and multiplying uncontrollably. They also help to repair damaged DNA and prevent the formation of tumors. Tumor suppressor proteins are encoded by genes that are located on specific chromosomes. When these genes are functioning properly, they produce proteins that help to regulate cell growth and prevent the development of cancer. However, when these genes are mutated or damaged, the proteins they produce may not function properly, leading to uncontrolled cell growth and the development of cancer. There are many different tumor suppressor proteins, each with its own specific function. Some of the most well-known tumor suppressor proteins include p53, BRCA1, and BRCA2. These proteins are involved in regulating cell cycle checkpoints, repairing damaged DNA, and preventing the formation of tumors. In summary, tumor suppressor proteins are a group of proteins that play a critical role in regulating cell growth and preventing the development of cancer. When these proteins are functioning properly, they help to maintain the normal balance of cell growth and division, but when they are mutated or damaged, they can contribute to the development of cancer.

The cell cycle is the series of events that a cell undergoes from the time it is born until it divides into two daughter cells. It is a highly regulated process that is essential for the growth, development, and repair of tissues in the body. The cell cycle consists of four main phases: interphase, prophase, metaphase, and anaphase. During interphase, the cell grows and replicates its DNA in preparation for cell division. In prophase, the chromatin condenses into visible chromosomes, and the nuclear envelope breaks down. In metaphase, the chromosomes align at the center of the cell, and in anaphase, the sister chromatids separate and move to opposite poles of the cell. The cell cycle is tightly regulated by a complex network of proteins that ensure that the cell only divides when it is ready and that the daughter cells receive an equal share of genetic material. Disruptions in the cell cycle can lead to a variety of medical conditions, including cancer.

Tumor suppressor protein p14ARF, also known as p16INK4a, is a protein that plays a crucial role in regulating cell growth and preventing the development of cancer. It is encoded by the CDKN2A gene, which is located on chromosome 9. p14ARF functions as a tumor suppressor by inhibiting the activity of the oncogenic protein MDM2, which normally promotes the degradation of the tumor suppressor protein p53. When p14ARF is present, it binds to MDM2 and prevents it from binding to p53, allowing p53 to accumulate and activate its tumor suppressive functions, such as promoting cell cycle arrest, DNA repair, and apoptosis (programmed cell death). Mutations in the CDKN2A gene can lead to a loss of p14ARF function, which can contribute to the development of various types of cancer, including lung cancer, pancreatic cancer, and melanoma. Therefore, p14ARF is considered a tumor suppressor protein and its function is important for maintaining normal cell growth and preventing the development of cancer.

Cell differentiation is the process by which cells acquire specialized functions and characteristics during development. It is a fundamental process that occurs in all multicellular organisms, allowing cells to differentiate into various types of cells with specific functions, such as muscle cells, nerve cells, and blood cells. During cell differentiation, cells undergo changes in their shape, size, and function, as well as changes in the proteins and other molecules they produce. These changes are controlled by a complex network of genes and signaling pathways that regulate the expression of specific genes in different cell types. Cell differentiation is a critical process for the proper development and function of tissues and organs in the body. It is also involved in tissue repair and regeneration, as well as in the progression of diseases such as cancer, where cells lose their normal differentiation and become cancerous.

Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (PTL) is a type of cancer that affects the white blood cells, specifically the T-cells. It is a rare and aggressive form of leukemia that occurs in children and young adults. PTL is characterized by the rapid growth of abnormal T-cells in the bone marrow, which leads to a decrease in the production of normal blood cells. This can cause symptoms such as fatigue, weakness, fever, and infections. The exact cause of PTL is not known, but it is believed to be related to genetic mutations that affect the normal development and function of T-cells. Treatment for PTL typically involves chemotherapy, radiation therapy, and stem cell transplantation. The prognosis for PTL varies depending on the age and overall health of the patient, as well as the stage and aggressiveness of the cancer.

Avian leukosis virus (ALV) is a type of retrovirus that infects birds, including chickens, turkeys, and ducks. It is a highly contagious virus that can cause a range of diseases in birds, including leukosis (cancer), lymphoid hyperplasia (enlargement of the lymph nodes), and immunosuppression (weakening of the immune system). There are several different subtypes of ALV, including avian leukosis virus subgroup J (ALV-J), which is the most common subtype found in chickens and turkeys. ALV-J can cause a variety of diseases in birds, including leukosis, lymphoid hyperplasia, and immunosuppression. It can also be transmitted to humans through contact with infected birds or their products, although human infections are rare. In the medical field, ALV is studied as a model for retroviral infections and as a potential source of therapeutic agents, such as antiviral drugs and vaccines. It is also an important consideration for the poultry industry, as ALV infections can cause significant economic losses through reduced productivity and increased mortality in infected birds.

Lung neoplasms refer to abnormal growths or tumors that develop in the lungs. These growths can be either benign (non-cancerous) or malignant (cancerous). Lung neoplasms can occur in any part of the lung, including the bronchi, bronchioles, and alveoli. Lung neoplasms can be further classified based on their type, including: 1. Primary lung neoplasms: These are tumors that develop in the lungs and do not spread to other parts of the body. 2. Secondary lung neoplasms: These are tumors that develop in the lungs as a result of cancer that has spread from another part of the body. 3. Benign lung neoplasms: These are non-cancerous tumors that do not spread to other parts of the body. 4. Malignant lung neoplasms: These are cancerous tumors that can spread to other parts of the body. Some common types of lung neoplasms include lung adenocarcinoma, squamous cell carcinoma, large cell carcinoma, and small cell carcinoma. The diagnosis of lung neoplasms typically involves a combination of imaging tests, such as chest X-rays and CT scans, and a biopsy to examine a sample of tissue from the tumor. Treatment options for lung neoplasms depend on the type, size, and location of the tumor, as well as the overall health of the patient.

Lymphoma is a type of cancer that affects the lymphatic system, which is a part of the immune system. It occurs when lymphocytes, a type of white blood cell, grow and divide uncontrollably, forming abnormal masses or tumors in the lymph nodes, spleen, bone marrow, or other parts of the body. There are two main types of lymphoma: Hodgkin lymphoma and non-Hodgkin lymphoma. Hodgkin lymphoma is a less common type of lymphoma that typically affects younger adults and has a better prognosis than non-Hodgkin lymphoma. Non-Hodgkin lymphoma is a more common type of lymphoma that can affect people of all ages and has a wide range of outcomes depending on the specific subtype and the stage of the disease. Symptoms of lymphoma can include swollen lymph nodes, fever, night sweats, weight loss, fatigue, and itching. Diagnosis typically involves a combination of physical examination, blood tests, imaging studies, and a biopsy of the affected tissue. Treatment for lymphoma depends on the subtype, stage, and overall health of the patient. It may include chemotherapy, radiation therapy, targeted therapy, immunotherapy, or a combination of these approaches. In some cases, a stem cell transplant may also be necessary.

Proto-oncogene proteins c-raf, also known as RAS-activating factor (RAF) or serine/threonine-protein kinase c-raf, are a family of proteins that play a critical role in regulating cell growth and division. They are encoded by the "raf" gene and are involved in the RAS/MAPK signaling pathway, which is a key pathway in cell proliferation, differentiation, and survival. In normal cells, the activity of c-raf proteins is tightly regulated, but mutations in the "raf" gene can lead to the overexpression or constitutive activation of these proteins, which can contribute to the development of cancer. Specifically, mutations in the "BRAF" gene, which encodes the B-Raf protein, are commonly found in several types of cancer, including melanoma, thyroid cancer, and colorectal cancer. In the medical field, c-raf proteins are often targeted for therapeutic intervention in cancer treatment. For example, small molecule inhibitors of the B-Raf protein have been developed and are currently being used in the treatment of certain types of cancer. Additionally, research is ongoing to develop new therapies that target other members of the c-raf family of proteins.

Nuclear proteins are proteins that are found within the nucleus of a cell. The nucleus is the control center of the cell, where genetic material is stored and regulated. Nuclear proteins play a crucial role in many cellular processes, including DNA replication, transcription, and gene regulation. There are many different types of nuclear proteins, each with its own specific function. Some nuclear proteins are involved in the structure and organization of the nucleus itself, while others are involved in the regulation of gene expression. Nuclear proteins can also interact with other proteins, DNA, and RNA molecules to carry out their functions. In the medical field, nuclear proteins are often studied in the context of diseases such as cancer, where changes in the expression or function of nuclear proteins can contribute to the development and progression of the disease. Additionally, nuclear proteins are important targets for drug development, as they can be targeted to treat a variety of diseases.

DNA, or deoxyribonucleic acid, is a molecule that carries genetic information in living organisms. It is composed of four types of nitrogen-containing molecules called nucleotides, which are arranged in a specific sequence to form the genetic code. In the medical field, DNA is often studied as a tool for understanding and diagnosing genetic disorders. Genetic disorders are caused by changes in the DNA sequence that can affect the function of genes, leading to a variety of health problems. By analyzing DNA, doctors and researchers can identify specific genetic mutations that may be responsible for a particular disorder, and develop targeted treatments or therapies to address the underlying cause of the condition. DNA is also used in forensic science to identify individuals based on their unique genetic fingerprint. This is because each person's DNA sequence is unique, and can be used to distinguish one individual from another. DNA analysis is also used in criminal investigations to help solve crimes by linking DNA evidence to suspects or victims.

Retroviridae proteins are a group of proteins that are encoded by retroviruses, which are a type of virus that can integrate their genetic material into the host cell's genome. These proteins play important roles in the life cycle of retroviruses, including the replication of the viral genome, the assembly of new virus particles, and the infection of new host cells. Some of the key retroviral proteins include: * Reverse transcriptase: This enzyme is responsible for converting the viral RNA genome into DNA, which can then be integrated into the host cell's genome. * Integrase: This enzyme is responsible for integrating the viral DNA into the host cell's genome. * Protease: This enzyme is responsible for processing the viral polyproteins into their individual components, which are then used to assemble new virus particles. * Gag protein: This protein is involved in the assembly of new virus particles. * Env protein: This protein is involved in the attachment of the virus to the host cell and the fusion of the viral envelope with the host cell membrane. Retroviridae proteins are important targets for the development of antiretroviral drugs, which are used to treat HIV and other retroviral infections.

Cyclin-dependent kinase inhibitor p16, also known as CDKN2A or p16INK4a, is a protein that plays a crucial role in regulating the cell cycle and preventing uncontrolled cell growth. It is encoded by the CDKN2A gene and is a member of the cyclin-dependent kinase inhibitor (CKI) family. In normal cells, p16 is expressed in response to DNA damage and acts as a brake on the cell cycle by inhibiting the activity of cyclin-dependent kinases (CDKs), which are enzymes that control cell cycle progression. When cells are damaged, p16 is activated and binds to CDK4 and CDK6, preventing them from phosphorylating and activating the retinoblastoma protein (Rb), which is a key regulator of the cell cycle. However, in many types of cancer, the CDKN2A gene is mutated or deleted, leading to a loss of p16 expression and allowing cells to bypass the cell cycle checkpoint controlled by p16. This can result in uncontrolled cell growth and the development of tumors. Therefore, p16 is considered a tumor suppressor gene, and its loss of function is associated with an increased risk of developing various types of cancer, including melanoma, lung cancer, and pancreatic cancer. In addition, p16 is also used as a diagnostic and prognostic marker in cancer, as its expression levels can be used to predict the aggressiveness of tumors and the response to treatment.

Skin neoplasms refer to abnormal growths or tumors that develop on the skin. These growths can be benign (non-cancerous) or malignant (cancerous). Skin neoplasms can occur anywhere on the body and can vary in size, shape, and color. Some common types of skin neoplasms include basal cell carcinoma, squamous cell carcinoma, melanoma, and keratosis. These growths can be treated with a variety of methods, including surgery, radiation therapy, chemotherapy, and immunotherapy. It is important to have any unusual skin growths evaluated by a healthcare professional to determine the best course of treatment.

Adenovirus early proteins are a group of proteins that are produced early in the infection cycle of an adenovirus. These proteins play important roles in the replication and spread of the virus within the host cell. They are synthesized from the viral genome as soon as it is replicated and before the production of the late proteins that are necessary for the assembly and release of new virus particles. The early proteins include the E1A and E1B proteins, which are essential for the transformation of host cells and the production of progeny virus. Other early proteins include the E2, E3, and E4 proteins, which have a variety of functions, including regulation of viral gene expression, modulation of host cell signaling pathways, and promotion of viral replication.

Fibroblast Growth Factor 3 (FGF3) is a protein that plays a role in cell growth, differentiation, and development. It is a member of the fibroblast growth factor family, which includes a group of proteins that regulate various cellular processes, including cell proliferation, migration, and differentiation. In the medical field, FGF3 has been studied in relation to a number of different conditions, including cancer, developmental disorders, and neurological disorders. For example, FGF3 has been shown to be involved in the development of certain types of cancer, such as breast cancer and colon cancer, and may play a role in the progression of these diseases. It has also been implicated in the development of certain developmental disorders, such as congenital heart defects and skeletal abnormalities, and may play a role in the development of neurological disorders, such as autism spectrum disorder. Overall, FGF3 is an important protein that plays a role in a variety of cellular processes and has been the subject of extensive research in the medical field.

Breast neoplasms refer to abnormal growths or tumors in the breast tissue. These growths can be benign (non-cancerous) or malignant (cancerous). Benign breast neoplasms are usually not life-threatening, but they can cause discomfort or cosmetic concerns. Malignant breast neoplasms, on the other hand, can spread to other parts of the body and are considered a serious health threat. Some common types of breast neoplasms include fibroadenomas, ductal carcinoma in situ (DCIS), invasive ductal carcinoma, and invasive lobular carcinoma.

Alpharetroviruses are a group of retroviruses that belong to the family Retroviridae. They are characterized by their single-stranded RNA genome and their ability to integrate into the host cell's DNA, where they can remain latent for long periods of time and be reactivated later to produce new virus particles. Alpharetroviruses are known to cause a variety of diseases in humans and animals, including leukemia, lymphoma, and neurodegenerative disorders. Some of the most well-known alpharetroviruses include the human T-cell leukemia virus type 1 (HTLV-1), which can cause adult T-cell leukemia/lymphoma, and the feline leukemia virus (FeLV), which can cause feline leukemia in cats. In addition to their role in disease, alpharetroviruses have also been studied as potential vectors for gene therapy, as they can efficiently deliver genetic material into cells and integrate into the host genome. However, the potential risks associated with viral vector-based gene therapy, including the possibility of insertional mutagenesis and oncogenesis, have led to increased caution in the use of alpharetroviruses and other retroviruses for this purpose.

Blotting, Southern is a laboratory technique used to detect specific DNA sequences in a sample. It is named after Edwin Southern, who developed the technique in the 1970s. The technique involves transferring DNA from a gel onto a membrane, such as nitrocellulose or nylon, and then using labeled probes to detect specific DNA sequences. The blotting process is often used in molecular biology research to study gene expression, genetic variation, and other aspects of DNA biology.

Proto-oncogene proteins c-jun are a family of proteins that play a role in cell proliferation, differentiation, and survival. They are encoded by the JUN gene and are members of the AP-1 transcription factor family. In normal cells, c-jun is involved in regulating the expression of genes that control cell growth and differentiation. However, when c-jun is mutated or overexpressed, it can contribute to the development of cancer. Proto-oncogene proteins c-jun are therefore considered to be proto-oncogenes, which are genes that have the potential to cause cancer when they are altered in some way.

Fusion proteins, specifically BCR-ABL, are a type of abnormal protein that occurs as a result of a genetic mutation in certain types of leukemia and other blood disorders. The BCR-ABL fusion protein is formed when two separate genes, BCR (breakpoint cluster region) and ABL (abelson murine leukemia virus), fuse together and become a single gene. This fusion gene is then expressed as a single protein, which is known as BCR-ABL. BCR-ABL is a tyrosine kinase, which is an enzyme that is involved in regulating cell growth and division. In the case of BCR-ABL, the abnormal activity of the fusion protein leads to uncontrolled cell growth and division, which can result in the development of leukemia or other blood disorders. BCR-ABL is typically diagnosed through a blood test that detects the presence of the fusion protein in the blood. Treatment for BCR-ABL-positive leukemia typically involves the use of targeted therapies, such as tyrosine kinase inhibitors, which are designed to specifically block the activity of the BCR-ABL fusion protein and prevent it from promoting uncontrolled cell growth and division.

Cloning, molecular, in the medical field refers to the process of creating identical copies of a specific DNA sequence or gene. This is achieved through a technique called polymerase chain reaction (PCR), which amplifies a specific DNA sequence to produce multiple copies of it. Molecular cloning is commonly used in medical research to study the function of specific genes, to create genetically modified organisms for therapeutic purposes, and to develop new drugs and treatments. It is also used in forensic science to identify individuals based on their DNA. In the context of human cloning, molecular cloning is used to create identical copies of a specific gene or DNA sequence from one individual and insert it into the genome of another individual. This technique has been used to create transgenic animals, but human cloning is currently illegal in many countries due to ethical concerns.

Comparative Genomic Hybridization (CGH) is a molecular genetic technique used to compare the DNA content of two or more samples. It is commonly used in the medical field to identify genetic changes or abnormalities in a sample, such as deletions, duplications, or amplifications of specific regions of DNA. In CGH, a reference sample of normal DNA is labeled with a fluorescent dye, and the sample of interest is also labeled with a different fluorescent dye. The two samples are then mixed and hybridized to a microarray, which is a slide containing thousands of small DNA fragments from a reference genome. The microarray is then scanned to detect any differences in the intensity of the fluorescent signals between the two samples. CGH can be used to detect genetic changes in a variety of settings, including cancer research, genetic counseling, and prenatal diagnosis. It is particularly useful for identifying copy number variations (CNVs), which are changes in the number of copies of a specific region of DNA. CNVs can be associated with a wide range of genetic disorders and diseases, including cancer, developmental disorders, and neurological disorders.

Proto-oncogene proteins c-pim-1, also known as Pim-1, are a family of serine/threonine kinases that play a role in cell proliferation, survival, and differentiation. They are encoded by the PIM1 gene and are expressed in a variety of tissues, including the hematopoietic system, the brain, and the liver. Pim-1 is involved in the regulation of cell cycle progression, apoptosis, and the response to DNA damage. It has been implicated in the development of various types of cancer, including leukemia, lymphoma, and solid tumors. In addition, Pim-1 has been shown to play a role in the development of resistance to chemotherapy and radiation therapy in some cancer cells. Targeting Pim-1 has been proposed as a potential therapeutic strategy for the treatment of cancer. Several small molecule inhibitors of Pim-1 have been developed and are currently being tested in preclinical and clinical studies.

Blotting, Northern is a laboratory technique used to detect and quantify specific RNA molecules in a sample. It involves transferring RNA from a gel onto a membrane, which is then hybridized with a labeled complementary DNA probe. The probe binds to the specific RNA molecules on the membrane, allowing their detection and quantification through autoradiography or other imaging methods. Northern blotting is commonly used to study gene expression patterns in cells or tissues, and to compare the expression levels of different RNA molecules in different samples.

Proto-oncogene proteins c-ret is a protein that is involved in the development and progression of cancer. It is a member of the receptor tyrosine kinase (RTK) family of proteins, which are involved in cell growth, differentiation, and survival. The c-ret protein is encoded by the RET gene, which is located on chromosome 10. Mutations in the RET gene can lead to the production of a constitutively active c-ret protein, which can cause uncontrolled cell growth and the development of cancer. The c-ret protein is primarily found in cells of the nervous system, but it has also been found in other types of cells, including those in the thyroid gland, lung, and kidney.

Carcinoma is a type of cancer that originates in the epithelial cells, which are the cells that line the surfaces of organs and tissues in the body. Carcinomas can develop in any part of the body, but they are most common in the skin, lungs, breast, prostate, and colon. Carcinomas are classified based on the location and type of epithelial cells from which they originate. For example, a carcinoma that develops in the skin is called a skin carcinoma, while a carcinoma that develops in the lungs is called a lung carcinoma. Carcinomas can be further classified as either non-melanoma skin cancers (such as basal cell carcinoma and squamous cell carcinoma) or melanoma, which is a more aggressive type of skin cancer that can spread to other parts of the body. Treatment for carcinomas depends on the type and stage of the cancer, as well as the overall health of the patient. Treatment options may include surgery, radiation therapy, chemotherapy, targeted therapy, or immunotherapy.

Leukemia is a type of cancer that affects the blood and bone marrow. It is characterized by the abnormal production of white blood cells, which can interfere with the normal functioning of the immune system and other parts of the body. There are several different types of leukemia, including acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML). Treatment for leukemia typically involves chemotherapy, radiation therapy, and/or stem cell transplantation.

Abelson murine leukemia virus (A-MuLV) is a type of retrovirus that infects mice and causes a form of leukemia. It was the first retrovirus to be discovered and was named after Dr. David Baltimore, who first identified it in 1970. A-MuLV is a type of helper virus, which means that it relies on another virus, called a packaging virus, to produce infectious particles. It is also a type of oncovirus, which means that it has the ability to cause cancer. Infection with A-MuLV can lead to the development of various types of leukemia, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML).

In the medical field, an amino acid sequence refers to the linear order of amino acids in a protein molecule. Proteins are made up of chains of amino acids, and the specific sequence of these amino acids determines the protein's structure and function. The amino acid sequence is determined by the genetic code, which is a set of rules that specifies how the sequence of nucleotides in DNA is translated into the sequence of amino acids in a protein. Each amino acid is represented by a three-letter code, and the sequence of these codes is the amino acid sequence of the protein. The amino acid sequence is important because it determines the protein's three-dimensional structure, which in turn determines its function. Small changes in the amino acid sequence can have significant effects on the protein's structure and function, and this can lead to diseases or disorders. For example, mutations in the amino acid sequence of a protein involved in blood clotting can lead to bleeding disorders.

Carcinogens are substances or agents that have the potential to cause cancer. They can be found in various forms, including chemicals, radiation, and biological agents. Carcinogens can be classified into two categories: 1. Direct carcinogens: These are substances that can directly damage DNA and cause mutations, leading to the development of cancer. Examples of direct carcinogens include tobacco smoke, asbestos, and ultraviolet radiation. 2. Indirect carcinogens: These are substances that do not directly damage DNA but can cause cancer by promoting the growth and survival of cancer cells. Examples of indirect carcinogens include certain hormones, viruses, and certain chemicals found in food and water. Carcinogens can cause cancer by disrupting the normal functioning of cells, leading to uncontrolled growth and division. Exposure to carcinogens can occur through various means, including inhalation, ingestion, or skin contact. The risk of developing cancer from exposure to carcinogens depends on several factors, including the type and duration of exposure, the individual's age and overall health, and their genetic makeup.

Cyclin D1 is a protein that plays a critical role in regulating the progression of the cell cycle from the G1 phase to the S phase. It is encoded by the CCND1 gene and is expressed in a variety of tissues, including epithelial cells, fibroblasts, and leukocytes. In the cell cycle, cyclin D1 binds to and activates cyclin-dependent kinases (CDKs), particularly CDK4 and CDK6. This complex then phosphorylates retinoblastoma protein (Rb), which releases the transcription factor E2F from its inhibition. E2F then activates the transcription of genes required for DNA synthesis and cell proliferation. Abnormal expression or activity of cyclin D1 has been implicated in the development of various types of cancer, including breast, prostate, and lung cancer. Overexpression of cyclin D1 can lead to uncontrolled cell proliferation and the formation of tumors. Conversely, loss of cyclin D1 function has been associated with cell cycle arrest and the development of cancer.

Blotting, Western is a laboratory technique used to detect specific proteins in a sample by transferring proteins from a gel to a membrane and then incubating the membrane with a specific antibody that binds to the protein of interest. The antibody is then detected using an enzyme or fluorescent label, which produces a visible signal that can be quantified. This technique is commonly used in molecular biology and biochemistry to study protein expression, localization, and function. It is also used in medical research to diagnose diseases and monitor treatment responses.

Retinoblastoma protein (pRb) is a tumor suppressor protein that plays a critical role in regulating cell cycle progression and preventing the development of cancer. It is encoded by the RB1 gene, which is located on chromosome 13. In normal cells, pRb functions as a regulator of the cell cycle by binding to and inhibiting the activity of the E2F family of transcription factors. When cells are damaged or under stress, pRb is phosphorylated, which leads to its release from E2F and allows the cell to proceed through the cell cycle and divide. However, in cells with a mutated RB1 gene, pRb is unable to function properly, leading to uncontrolled cell division and the formation of tumors. Retinoblastoma is a type of eye cancer that occurs almost exclusively in children and is caused by mutations in the RB1 gene. Other types of cancer, such as osteosarcoma and small cell lung cancer, can also be associated with mutations in the RB1 gene.

Carcinoma, Squamous Cell is a type of cancer that originates in the squamous cells, which are thin, flat cells that line the surface of the body. Squamous cells are found in the skin, mouth, throat, lungs, and other organs. Carcinoma, Squamous Cell can develop in any part of the body where squamous cells are present, but it is most commonly found in the head and neck, lungs, and skin. The exact cause of Squamous Cell Carcinoma is not always clear, but it is often associated with exposure to certain substances, such as tobacco smoke, alcohol, and certain chemicals. It can also develop as a result of chronic inflammation or infection, such as HPV (human papillomavirus) infection in the cervix. Symptoms of Squamous Cell Carcinoma can vary depending on the location of the tumor, but may include a persistent sore or lesion that does not heal, a change in the appearance of the skin or mucous membranes, difficulty swallowing or breathing, and unexplained weight loss. Treatment for Squamous Cell Carcinoma typically involves surgery to remove the tumor, followed by radiation therapy or chemotherapy to kill any remaining cancer cells. In some cases, targeted therapy or immunotherapy may also be used. The prognosis for Squamous Cell Carcinoma depends on the stage of the cancer at the time of diagnosis and the overall health of the patient.

The Epidermal Growth Factor Receptor (EGFR) is a type of cell surface receptor protein that is found on the surface of cells in the epidermis, as well as in other tissues throughout the body. The EGFR is a member of a family of receptors called receptor tyrosine kinases, which are involved in regulating cell growth, differentiation, and survival. When the EGFR binds to its ligand, a protein called epidermal growth factor (EGF), it triggers a cascade of intracellular signaling events that ultimately lead to the activation of various genes involved in cell growth and proliferation. This process is important for normal tissue growth and repair, but it can also contribute to the development of cancer when the EGFR is overactive or mutated. EGFR inhibitors are a class of drugs that are used to treat certain types of cancer, such as non-small cell lung cancer and head and neck cancer, by blocking the activity of the EGFR and preventing it from signaling downstream genes. These drugs can be used alone or in combination with other treatments, such as chemotherapy or radiation therapy.

Isobutyrates are a group of organic compounds that contain a carboxyl group (-COOH) and an isobutyl group (-C4H9). They are derivatives of butyric acid, which is a short-chain fatty acid found in the gut and produced by the breakdown of dietary fats. In the medical field, isobutyrates are used as intermediates in the production of various pharmaceuticals and chemicals. They are also used as solvents, plasticizers, and flavoring agents in the food and beverage industry. One specific isobutyrate that has gained attention in recent years is isobutyl acetate, which is a common solvent used in the production of pharmaceuticals and cosmetics. It has been shown to have potential anti-inflammatory and analgesic effects, and is being studied for its potential use in the treatment of various conditions such as arthritis and pain.

Phosphatidylinositol 3-kinases (PI3Ks) are a family of enzymes that play a critical role in cellular signaling pathways. They are involved in a wide range of cellular processes, including cell growth, proliferation, differentiation, survival, migration, and metabolism. PI3Ks are activated by various extracellular signals, such as growth factors, hormones, and neurotransmitters, and they generate second messengers by phosphorylating phosphatidylinositol lipids on the inner leaflet of the plasma membrane. This leads to the recruitment and activation of downstream effector molecules, such as protein kinases and phosphatases, which regulate various cellular processes. Dysregulation of PI3K signaling has been implicated in the development of various diseases, including cancer, diabetes, and neurological disorders. Therefore, PI3Ks are important targets for the development of therapeutic agents for these diseases.

Mammary Neoplasms, Experimental refers to the study of neoplasms (tumors) that occur in the mammary glands of animals, typically laboratory animals such as mice, rats, and rabbits. These studies are conducted in a controlled laboratory setting to understand the development, progression, and potential treatment of mammary tumors in humans. The animals are typically genetically modified or treated with various chemicals or hormones to induce the development of mammary tumors. The results of these studies can provide valuable information for the development of new treatments for breast cancer in humans.

Protein-Serine-Threonine Kinases (PSTKs) are a family of enzymes that play a crucial role in regulating various cellular processes, including cell growth, differentiation, metabolism, and apoptosis. These enzymes phosphorylate specific amino acids, such as serine and threonine, on target proteins, thereby altering their activity, stability, or localization within the cell. PSTKs are involved in a wide range of diseases, including cancer, diabetes, cardiovascular disease, and neurodegenerative disorders. Therefore, understanding the function and regulation of PSTKs is important for developing new therapeutic strategies for these diseases.

In the medical field, "chickens" typically refers to the domesticated bird species Gallus gallus domesticus. Chickens are commonly raised for their meat, eggs, and feathers, and are also used in research and as pets. In veterinary medicine, chickens can be treated for a variety of health conditions, including diseases such as avian influenza, Newcastle disease, and fowl pox. They may also require treatment for injuries or trauma, such as broken bones or cuts. In human medicine, chickens are not typically used as a source of treatment or therapy. However, some research has been conducted using chicken cells or proteins as models for human diseases or as potential sources of vaccines or other medical interventions.

Myeloid-Lymphoid Leukemia Protein (MLL) is a type of protein that plays a crucial role in the development and function of blood cells. It is also known as Mixed Lineage Leukemia (MLL) protein. MLL is a member of a family of proteins called histone methyltransferases, which are enzymes that add methyl groups to the tails of histone proteins. Histones are proteins that help package DNA into a compact structure called chromatin. By adding methyl groups to histones, MLL can affect the accessibility of DNA to the machinery that reads and writes genetic information, which in turn can influence gene expression. In the context of leukemia, mutations in the MLL gene can lead to the production of abnormal versions of the MLL protein that are not properly regulated. This can result in the uncontrolled growth and proliferation of blood cells, leading to the development of leukemia. MLL is a type of acute leukemia that affects both myeloid and lymphoid cells, hence the name "myeloid-lymphoid leukemia." It is a rare type of leukemia, accounting for only about 1-2% of all cases of acute leukemia. Treatment for MLL leukemia typically involves chemotherapy, stem cell transplantation, and targeted therapies that specifically target the abnormal MLL protein.

Carcinogenesis is the process by which normal cells in the body transform into cancer cells. It is a multi-step process that involves genetic and epigenetic changes that lead to the uncontrolled growth and division of cells, ultimately resulting in the formation of a tumor. Carcinogenesis can be caused by various factors, including exposure to carcinogens (substances that can cause cancer), genetic mutations, hormonal imbalances, and chronic inflammation. The process of carcinogenesis can take many years or even decades, and it can occur in any part of the body. Understanding the mechanisms of carcinogenesis is important for developing effective strategies for preventing and treating cancer. This includes identifying and avoiding carcinogenic substances, developing targeted therapies to inhibit the growth and spread of cancer cells, and developing early detection methods to identify cancer at an early stage when it is more treatable.

In the medical field, "Liver Neoplasms, Experimental" refers to the study of liver tumors or cancer in experimental settings, such as in laboratory animals or tissue cultures. This type of research is typically conducted to better understand the underlying mechanisms of liver cancer and to develop new treatments or therapies for the disease. Experimental liver neoplasms may involve the use of various techniques, such as genetic manipulation, drug administration, or exposure to environmental toxins, to induce the development of liver tumors in animals or cells. The results of these studies can provide valuable insights into the biology of liver cancer and inform the development of new diagnostic and therapeutic approaches for the disease.

In the medical field, "Chromosomes, Human, Pair 8" refers to the 8th pair of chromosomes in the human genome. Each pair of chromosomes contains a set of genes that are responsible for various traits and characteristics of an individual. The 8th pair of chromosomes is also known as chromosome 8 or chromosome 8p. Chromosome 8 is one of the largest human chromosomes, containing over 190 million base pairs of DNA. It is composed of two homologous chromosomes, one inherited from each parent. The genes located on chromosome 8 are involved in a wide range of biological processes, including cell growth and division, immune system function, and the development of certain diseases. Mutations or abnormalities in chromosome 8 can lead to a variety of genetic disorders, such as cri du chat syndrome, which is characterized by intellectual disability, delayed development, and a high-pitched cry. Additionally, certain genetic variations on chromosome 8 have been associated with an increased risk of certain types of cancer, such as breast and ovarian cancer.

Receptor Protein-Tyrosine Kinases (RPTKs) are a class of cell surface receptors that play a crucial role in cell signaling and communication. These receptors are transmembrane proteins that span the cell membrane and have an extracellular domain that binds to specific ligands, such as hormones, growth factors, or neurotransmitters. When a ligand binds to an RPTK, it triggers a conformational change in the receptor, which activates its intracellular tyrosine kinase domain. This domain then phosphorylates specific tyrosine residues on intracellular proteins, leading to the activation of downstream signaling pathways that regulate various cellular processes, such as cell growth, differentiation, migration, and survival. RPTKs are involved in many important physiological processes, including embryonic development, tissue repair, and immune responses. However, they can also contribute to the development of various diseases, including cancer, as mutations in RPTKs can lead to uncontrolled cell growth and proliferation. Therefore, RPTKs are an important target for the development of new therapeutic strategies for treating cancer and other diseases.

Chromosomal instability (CIN) is a condition in which cells have an increased tendency to experience errors during cell division, leading to the formation of abnormal chromosomes or aneuploidy. This can result in the production of cells with too many or too few chromosomes, which can lead to a variety of health problems, including cancer. CIN can be caused by a variety of factors, including genetic mutations, exposure to certain chemicals or radiation, and certain viral infections. It is often associated with the development of cancer, as the abnormal chromosomes produced by CIN can lead to the uncontrolled growth and division of cells. There are several different types of CIN, including constitutional chromosomal instability (CCI), which is present from birth and is associated with a higher risk of cancer, and acquired chromosomal instability (ACI), which is caused by environmental factors and is associated with a higher risk of cancer in adulthood. Treatment for CIN depends on the underlying cause and the specific symptoms and health problems associated with the condition. In some cases, treatment may involve medications or other therapies to help manage symptoms or prevent the development of cancer. In other cases, surgery or other interventions may be necessary to remove abnormal cells or tumors.

Thymus neoplasms refer to tumors that develop in the thymus gland, which is a small organ located in the upper chest, behind the breastbone. The thymus gland is responsible for the development and maturation of T-cells, which are a type of white blood cell that plays a critical role in the immune system. Thymus neoplasms can be either benign or malignant. Benign thymus neoplasms are non-cancerous and do not spread to other parts of the body. Malignant thymus neoplasms, on the other hand, are cancerous and can spread to other parts of the body, leading to serious health problems. Thymus neoplasms can be further classified based on their type, including thymoma, thymic carcinoma, and thymic hyperplasia. Thymoma is the most common type of thymus neoplasm, accounting for about 90% of all cases. Thymic carcinoma is a rare and aggressive type of thymus neoplasm, while thymic hyperplasia is a non-cancerous condition characterized by an overgrowth of thymus tissue. Thymus neoplasms can cause a variety of symptoms, including chest pain, difficulty breathing, coughing, and fatigue. Diagnosis typically involves imaging tests such as CT scans or MRI, as well as a biopsy to confirm the presence of a tumor. Treatment options for thymus neoplasms depend on the type and stage of the tumor, and may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

In the medical field, "cell survival" refers to the ability of cells to survive and continue to function despite exposure to harmful stimuli or conditions. This can include exposure to toxins, radiation, or other forms of stress that can damage or kill cells. Cell survival is an important concept in many areas of medicine, including cancer research, where understanding how cells survive and resist treatment is crucial for developing effective therapies. In addition, understanding the mechanisms that regulate cell survival can also have implications for other areas of medicine, such as tissue repair and regeneration.

Antineoplastic agents, also known as cytotoxic agents or chemotherapeutic agents, are drugs that are used to treat cancer by killing or slowing the growth of cancer cells. These agents work by interfering with the normal processes of cell division and growth, which are necessary for the survival and spread of cancer cells. There are many different types of antineoplastic agents, including alkylating agents, antimetabolites, topoisomerase inhibitors, and monoclonal antibodies, among others. These agents are often used in combination with other treatments, such as surgery and radiation therapy, to provide the most effective treatment for cancer.

Thyroid neoplasms refer to abnormal growths or tumors in the thyroid gland, which is a butterfly-shaped gland located in the neck. These neoplasms can be either benign (non-cancerous) or malignant (cancerous). Thyroid neoplasms can occur in any part of the thyroid gland, but some areas are more prone to developing tumors than others. The most common type of thyroid neoplasm is a thyroid adenoma, which is a benign tumor that arises from the follicular cells of the thyroid gland. Other types of thyroid neoplasms include papillary thyroid carcinoma, follicular thyroid carcinoma, medullary thyroid carcinoma, and anaplastic thyroid carcinoma. Thyroid neoplasms can cause a variety of symptoms, depending on the size and location of the tumor, as well as whether it is benign or malignant. Some common symptoms include a lump or swelling in the neck, difficulty swallowing, hoarseness, and a rapid or irregular heartbeat. Diagnosis of thyroid neoplasms typically involves a combination of physical examination, imaging studies such as ultrasound or CT scan, and biopsy of the thyroid tissue. Treatment options for thyroid neoplasms depend on the type, size, and location of the tumor, as well as the patient's overall health and age. Treatment may include surgery, radiation therapy, or medication to manage symptoms or slow the growth of the tumor.

DNA primers are short, single-stranded DNA molecules that are used in a variety of molecular biology techniques, including polymerase chain reaction (PCR) and DNA sequencing. They are designed to bind to specific regions of a DNA molecule, and are used to initiate the synthesis of new DNA strands. In PCR, DNA primers are used to amplify specific regions of DNA by providing a starting point for the polymerase enzyme to begin synthesizing new DNA strands. The primers are complementary to the target DNA sequence, and are added to the reaction mixture along with the DNA template, nucleotides, and polymerase enzyme. The polymerase enzyme uses the primers as a template to synthesize new DNA strands, which are then extended by the addition of more nucleotides. This process is repeated multiple times, resulting in the amplification of the target DNA sequence. DNA primers are also used in DNA sequencing to identify the order of nucleotides in a DNA molecule. In this application, the primers are designed to bind to specific regions of the DNA molecule, and are used to initiate the synthesis of short DNA fragments. The fragments are then sequenced using a variety of techniques, such as Sanger sequencing or next-generation sequencing. Overall, DNA primers are an important tool in molecular biology, and are used in a wide range of applications to study and manipulate DNA.

Notch1 is a type of receptor protein that plays a critical role in cell signaling and differentiation. It is a transmembrane protein that is expressed on the surface of many different types of cells, including neurons, immune cells, and cancer cells. In the medical field, Notch1 is of particular interest because it is involved in a number of important biological processes, including cell proliferation, differentiation, and apoptosis (programmed cell death). Abnormalities in Notch1 signaling have been linked to a variety of diseases, including cancer, developmental disorders, and immune system disorders. Notch1 signaling occurs when the receptor protein binds to a ligand protein on the surface of another cell. This binding event triggers a cascade of intracellular signaling events that ultimately lead to changes in gene expression and cellular behavior. In some cases, Notch1 signaling can promote cell proliferation and survival, while in other cases it can promote cell differentiation and death. In the context of cancer, Notch1 signaling has been implicated in the development and progression of a variety of different types of tumors, including breast cancer, lung cancer, and leukemia. In these cases, abnormal Notch1 signaling can contribute to the growth and spread of cancer cells, making it an important target for cancer therapy.

Chromosomes, Human, Pair 11 refers to the 11th pair of chromosomes in the human genome. Each pair of chromosomes contains a specific set of genes that are responsible for various traits and characteristics of an individual. Chromosome 11 is one of the largest human chromosomes, containing over 150 million base pairs of DNA and more than 1,000 genes. It is located on the long (q) arm of the chromosome and is known to be involved in the development and function of various organs and tissues, including the immune system, brain, and reproductive system. Mutations or abnormalities in chromosome 11 can lead to a variety of genetic disorders, such as cri du chat syndrome, velocardiofacial syndrome, and Smith-Magenis syndrome.

Telomerase is an enzyme that is responsible for maintaining the length of telomeres, which are the protective caps at the ends of chromosomes. Telomeres are essential for the proper functioning of chromosomes, as they prevent the loss of genetic information during cell division. In most cells, telomeres shorten with each cell division, eventually leading to cellular senescence or death. However, some cells, such as stem cells and cancer cells, are able to maintain their telomere length through the activity of telomerase. In the medical field, telomerase has been the subject of extensive research due to its potential as a therapeutic target for treating age-related diseases and cancer. For example, activating telomerase in cells has been shown to delay cellular senescence and extend the lifespan of cells in vitro. Additionally, inhibiting telomerase activity has been shown to be effective in treating certain types of cancer, as it can prevent cancer cells from dividing and spreading.

Proto-oncogene proteins c-bcl-2 are a family of proteins that play a role in regulating cell survival and apoptosis (programmed cell death). They are encoded by the bcl-2 gene, which is located on chromosome 18 in humans. The c-bcl-2 protein is a member of the Bcl-2 family of proteins, which are involved in regulating the balance between cell survival and death. The c-bcl-2 protein is a homodimer, meaning that it forms a pair of identical protein molecules that interact with each other. It is primarily found in the cytoplasm of cells, but it can also be found in the nucleus. The c-bcl-2 protein is thought to function as an anti-apoptotic protein, meaning that it inhibits the process of programmed cell death. It does this by preventing the release of cytochrome c from the mitochondria, which is a key step in the activation of the apoptotic pathway. In addition, the c-bcl-2 protein can also promote cell survival by inhibiting the activity of pro-apoptotic proteins. Abnormal expression of the c-bcl-2 protein has been implicated in the development of various types of cancer, including lymphoma, leukemia, and ovarian cancer. In these cases, overexpression of the c-bcl-2 protein can lead to increased cell survival and resistance to apoptosis, which can contribute to the growth and progression of cancer.

Chromosome mapping is a technique used in genetics to identify the location of genes on chromosomes. It involves analyzing the physical and genetic characteristics of chromosomes to determine their structure and organization. This information can be used to identify genetic disorders, understand the inheritance patterns of traits, and develop new treatments for genetic diseases. Chromosome mapping can be done using various techniques, including karyotyping, fluorescence in situ hybridization (FISH), and array comparative genomic hybridization (array CGH).

Receptor, erbB-2, also known as HER2 or neu, is a protein that is found on the surface of certain cells in the human body. It is a type of receptor tyrosine kinase, which means that it is a protein that is activated when it binds to a specific molecule, called a ligand. In the case of erbB-2, the ligand is a protein called epidermal growth factor (EGF). ErbB-2 is involved in a number of important cellular processes, including cell growth, differentiation, and survival. It is also a key player in the development of certain types of cancer, particularly breast cancer. In some cases, the erbB-2 gene may be overexpressed or mutated, leading to an overabundance of the erbB-2 protein on the surface of cancer cells. This can contribute to the uncontrolled growth and spread of the cancer. There are several ways that doctors can test for erbB-2 overexpression in breast cancer patients. One common method is to use a test called immunohistochemistry (IHC), which involves staining tissue samples with an antibody that binds specifically to the erbB-2 protein. If the erbB-2 protein is present in high levels, the tissue will appear dark under the microscope. Another method is to use a test called fluorescence in situ hybridization (FISH), which involves using a fluorescent probe to detect the presence of the erbB-2 gene on the cancer cells. If a patient's breast cancer is found to be positive for erbB-2 overexpression, they may be eligible for treatment with drugs called trastuzumab (Herceptin) or pertuzumab (Perjeta), which are designed to target the erbB-2 protein and help to shrink or stop the growth of the cancer. These drugs are often used in combination with other treatments, such as chemotherapy or radiation therapy.

Proto-oncogene proteins c-fos are a group of proteins that play a role in cell growth and differentiation. They are encoded by the c-fos gene and are involved in the regulation of cell proliferation, differentiation, and survival. In normal cells, c-fos proteins are expressed at low levels and play a role in the regulation of cell growth and differentiation. However, in cancer cells, the expression of c-fos proteins is often increased, leading to uncontrolled cell growth and the development of cancer. Proto-oncogene proteins c-fos are therefore considered to be oncogenes, which are genes that have the potential to cause cancer.

Neoplasms, radiation-induced are abnormal growths of cells that are caused by exposure to ionizing radiation. Ionizing radiation is a type of energy that has enough force to remove tightly bound electrons from atoms, causing the atoms to become ionized. This type of radiation is capable of damaging DNA and other cellular structures, which can lead to mutations and the development of cancer. Radiation-induced neoplasms can occur in any part of the body that has been exposed to ionizing radiation, including the skin, lungs, thyroid gland, and bone marrow. The risk of developing a radiation-induced neoplasm increases with the dose of radiation received and the duration of exposure. In addition, certain factors such as age, gender, and genetic predisposition can also affect the risk of developing a radiation-induced neoplasm. Treatment for radiation-induced neoplasms depends on the type and stage of the cancer, as well as the location and extent of the radiation exposure. Options may include surgery, radiation therapy, chemotherapy, and targeted therapy. It is important for individuals who have been exposed to ionizing radiation to be monitored for the development of radiation-induced neoplasms, as early detection and treatment can improve outcomes.

Melanoma is a type of skin cancer that begins in the cells that produce the pigment melanin. It is the most dangerous type of skin cancer, as it has the potential to spread to other parts of the body and be difficult to treat. Melanoma can occur in any part of the body, but it most commonly appears on the skin as a new mole or a change in an existing mole. Other signs of melanoma may include a mole that is asymmetrical, has irregular borders, is a different color than the surrounding skin, is larger than a pencil eraser, or has a raised or scaly surface. Melanoma can also occur in the eye, mouth, and other parts of the body, and it is important to see a doctor if you have any concerning changes in your skin or other parts of your body.

Liver neoplasms refer to abnormal growths or tumors that develop in the liver. These growths can be either benign (non-cancerous) or malignant (cancerous). Benign liver neoplasms include hemangiomas, focal nodular hyperplasia, and adenomas. These growths are usually slow-growing and do not spread to other parts of the body. Malignant liver neoplasms, on the other hand, are more serious and include primary liver cancer (such as hepatocellular carcinoma) and secondary liver cancer (such as metastatic cancer from other parts of the body). These tumors can grow quickly and spread to other parts of the body, leading to serious health complications. Diagnosis of liver neoplasms typically involves imaging tests such as ultrasound, CT scan, or MRI, as well as blood tests and biopsy. Treatment options depend on the type and stage of the neoplasm, and may include surgery, chemotherapy, radiation therapy, or targeted therapy.

In the medical field, a codon is a sequence of three nucleotides (adenine, cytosine, guanine, thymine, or uracil) that codes for a specific amino acid in a protein. There are 64 possible codons, and each one corresponds to one of the 20 amino acids used to build proteins. The sequence of codons in a gene determines the sequence of amino acids in the resulting protein, which ultimately determines the protein's structure and function. Mutations in a gene can change the codon sequence, which can lead to changes in the amino acid sequence and potentially affect the function of the protein.

Avian proteins refer to proteins that are derived from birds. In the medical field, avian proteins are often used as a source of therapeutic agents, such as antibodies and growth factors, for the treatment of various diseases. For example, chicken egg white lysozyme is used as an antibiotic in ophthalmology, and chicken serum albumin is used as a plasma expander in surgery. Additionally, avian proteins are also used in the development of vaccines and diagnostic tests.

Adenocarcinoma is a type of cancer that starts in the glandular cells of an organ or tissue. It is one of the most common types of cancer and can occur in many different parts of the body, including the lungs, breast, colon, rectum, pancreas, stomach, and thyroid gland. Adenocarcinomas typically grow slowly and may not cause symptoms in the early stages. However, as the cancer grows, it can invade nearby tissues and spread to other parts of the body through the bloodstream or lymphatic system. This can lead to more serious symptoms and a higher risk of complications. Treatment for adenocarcinoma depends on the location and stage of the cancer, as well as the overall health of the patient. Options may include surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these approaches. The goal of treatment is to remove or destroy the cancer cells and prevent them from spreading further.

In the medical field, "trans-activators" refer to proteins or molecules that activate the transcription of a gene, which is the process by which the information in a gene is used to produce a functional product, such as a protein. Trans-activators can bind to specific DNA sequences near a gene and recruit other proteins, such as RNA polymerase, to initiate transcription. They can also modify the chromatin structure around a gene to make it more accessible to transcription machinery. Trans-activators play important roles in regulating gene expression and are involved in many biological processes, including development, differentiation, and disease.

Avian Sarcoma Viruses (ASV) are a group of retroviruses that infect birds and can cause various types of tumors, including sarcomas, leukemias, and lymphomas. These viruses are transmitted from bird to bird through contact with bodily fluids, such as saliva, semen, and egg whites. ASVs are classified into two main groups: avian leukosis viruses (ALVs) and avian sarcoma-leukosis viruses (ASLVs). ALVs are further divided into subgroups based on their ability to induce tumors in chickens, turkeys, and ducks. ASLVs are also classified into subgroups based on their ability to induce tumors in different bird species. ASVs are of interest to researchers because they provide a model for studying the mechanisms of retroviral replication and oncogenesis. They have also been used as vectors for gene therapy and as a tool for studying the immune response to viral infections. However, ASVs can also be a significant problem for the poultry industry, as they can cause significant economic losses due to the development of tumors in birds.

In the medical field, "neoplasm invasiveness" refers to the ability of a cancerous tumor to invade and spread beyond its original site of origin. This can occur through the bloodstream or lymphatic system, or by direct extension into surrounding tissues. The degree of invasiveness of a neoplasm can be an important factor in determining the prognosis and treatment options for a patient. More invasive tumors are generally considered to be more aggressive and may be more difficult to treat. However, the specific characteristics of the tumor, such as its type, stage, and location, as well as the overall health of the patient, can also play a role in determining the prognosis. Invasive neoplasms may also be referred to as malignant tumors, as they have the potential to spread and cause harm to surrounding tissues and organs. Non-invasive neoplasms, on the other hand, are generally considered to be benign and are less likely to spread.

A proto-oncogene is a normal gene that could become an oncogene due to mutations or increased expression. Proto-oncogenes code ... Most oncogenes began as proto-oncogenes: normal genes involved in cell growth and proliferation or inhibition of apoptosis. If ... Many cancer drugs target the proteins encoded by oncogenes. Oncogenes are a physically and functionally diverse set of genes, ... The resultant protein encoded by an oncogene is termed oncoprotein. Oncogenes play an important role in the regulation or ...
Examples of inhibitors that have been used to block oncogenes and disrupt oncogene addiction include imatinib, nilotinib, ... Oncogene addiction is a process in which cancers with genetic, epigenetic, or chromosomal irregularities become dependent on ... As a result, cancer cells rely on continuous signaling from these oncogenes for their survival. The term was coined in 2002 by ... Oncogene inhibition typically results progression-free survival of a few months, meaning most cancer treatment ultimately ...
The MAS1 oncogene (MAS receptor) is a G protein-coupled receptor which binds the angiotensin II metabolite angiotensin (1-7). ... IUPHAR GPCR Database - MAS1 IUPHAR GPCR Database - MAS1L proto-oncogene+proteins+c-mas-1 at the U.S. National Library of ... Young D, Waitches G, Birchmeier C, Fasano O, Wigler M (June 1986). "Isolation and characterization of a new cellular oncogene ...
"Journal Information: Oncogene". Nature. Retrieved 2023-02-19. "About the Editors: Oncogene". Nature. Retrieved 2023-02-19. v t ... Nature Research List of Nature Research journals Miller G, Stebbing J (October 2018). "Thirty years of Oncogene". Oncogene. 37 ... Oncogene received a 2021 impact factor of 8.756 and received Journal Citation Reports rankings of 38th out of 245 journals in ... Oncogene is a peer-reviewed scientific journal published under the Nature Portfolio addressing cancer cell genetics and the ...
"Characterization of the ret proto-oncogene products expressed in mouse L cells". Oncogene. 8 (11): 2925-2929. PMID 8414495. ... RET proto-oncogene has been shown to interact with: DOK1, DOK5, GDNF family receptor alpha 1, GRB10, GRB7, Grb2, SHC1, and ... The RET proto-oncogene encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor (GDNF ... GeneReviews/NCBI/NIH/UW entry on Multiple Endocrine Neoplasia Type 2 ret+Proto-Oncogene+Proteins at the U.S. National Library ...
... , or Proto-oncogene Int-1 homolog is a protein that in humans is encoded by the WNT1 (INT1) gene. The WNT ... Arheden K, Mandahl N, Strombeck B, Isaksson M, Mitelman F (May 1988). "Chromosome localization of the human oncogene INT1 to ... van Ooyen A, Kwee V, Nusse R (Jan 1986). "The nucleotide sequence of the human int-1 mammary oncogene; evolutionary ... De Ferrari GV, Moon RT (2007). "The ups and downs of Wnt signaling in prevalent neurological disorders". Oncogene. 25 (57): ...
... is a protein that in humans is encoded by the MYBL1 gene. GRCh38: Ensembl release 89: ENSG00000185697 ... "Entrez Gene: MYB proto-oncogene like 1". Retrieved 2016-11-15. Ramkissoon LA, Horowitz PM, Craig JM, Ramkissoon SH, Rich BE, ...
The N-ras proto-oncogene is a member of the Ras gene family. It is mapped on chromosome 1, and it is activated in HL60, a ... Nitta N, Ochiai M, Nagao M, Sugimura T (1987). "Amino-acid substitution at codon 13 of the N-ras oncogene in rectal cancer in a ... 1984). "Mechanism of activation of an N-ras oncogene of SW-1271 human lung carcinoma cells". Proc. Natl. Acad. Sci. U.S.A. 81 ( ... 1988). "Analysis of RAS oncogene mutations in human lymphoid malignancies". Proc. Natl. Acad. Sci. U.S.A. 85 (23): 9268-72. ...
... , also known as proto-oncogene c-Src, or simply c-Src (cellular Src; pronounced "sarc ... Eventually this normal gene mutated into an abnormally functioning oncogene within the Rous sarcoma virus. Once the oncogene is ... This proto-oncogene may play a role in the regulation of embryonic development and cell growth. When src is activated, it ... "Entrez Gene: SRC v-src sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (avian)". Wheeler DL, Iida M, Dunn EF (July 2009). " ...
Oncogenes build up an inflammatory pro-tumorigenic microenvironment. Some hormones play a role in the development of cancer by ... Oncogenes are genes that promote cell growth and reproduction. Tumor suppressor genes are genes that inhibit cell division and ... A further mutation in an oncogene might cause the cell to reproduce more rapidly and more frequently than its normal ... Croce CM (January 2008). "Oncogenes and cancer". The New England Journal of Medicine. 358 (5): 502-11. doi:10.1056/NEJMra072367 ...
Croce CM (January 2008). "Oncogenes and cancer". N. Engl. J. Med. 358 (5): 502-11. doi:10.1056/NEJMra072367. PMID 18234754. ...
One of the first oncogenes to be defined in cancer research is the ras oncogene. Mutations in the Ras family of proto-oncogenes ... Mutations in proto-oncogenes, which are the normally quiescent counterparts of oncogenes, can modify their expression and ... Because viral genome insertion is not specific to proto-oncogenes and the chance of insertion near that proto-oncogene is low, ... It is only when enough proto-oncogenes have mutated into oncogenes, and enough tumor suppressor genes deactivated or damaged, ...
This addiction is part of a more general phenomenon involving oncogenes, called oncogene addiction. Studies have been performed ... Addiction to oncogenes--the Achilles heal of cancer". Science. 297 (5578): 63-4. doi:10.1126/science.1073096. PMID 12098689. ... Some oncomir genes are oncogenes, in that overexpression of the gene leads to cancerous growth. Other oncomir genes are tumor ... For example, in lung cancer some oncogenes are down-regulated by Let-7, which functions to maintain normal cell progression. ...
Abnormal amounts of gene product can be correlated with disease-causing alleles, such as the overactivity of oncogenes which ... Croce CM (January 2008). "Oncogenes and cancer". The New England Journal of Medicine. 358 (5): 502-11. doi:10.1056/NEJMra072367 ...
Bishop JM (1983). "Cellular oncogenes and retroviruses". Annu. Rev. Biochem. 52: 301-54. doi:10.1146/annurev.bi.52.070183. ...
Oncogenes: Stimulate cell proliferation. It is in this group where members of the RAS family are found. Oncogenes generally ... In the small GTPase family it is classified in the RAS domain, a special group of oncogenes and oncoproteins that take part in ... The basic members of this group of proteins are Ras oncogenes. It's divided into five major families (Ras, Rho, Arf/Sar, Ran ...
Oncogene. 9 (11): 3281-8. PMID 7936652. Chan AM, Miki T, Meyers KA, Aaronson SA (August 1994). "A human oncogene of the RAS ... Ras-related protein M-Ras, also known as muscle RAS oncogene homolog and R-Ras3, is a protein that in humans is encoded by the ... "Entrez Gene: MRAS muscle RAS oncogene homolog". "BioGPS - your Gene Portal System". biogps.org. Retrieved 2016-10-10.[permanent ... Karnoub AE, Weinberg RA (July 2008). "Ras oncogenes: split personalities". Nature Reviews Molecular Cell Biology. 9 (7): 517-31 ...
Oncogenes and cell proliferation. 15 (1): 102-111. doi:10.1016/j.gde.2004.12.005. PMID 15661540. Van den Brenk, H. A.; Crowe, M ...
Oncogene. England. 21 (42): 6488-97. doi:10.1038/sj.onc.1205840. ISSN 0950-9232. PMID 12226752. Bowman, A B; Kamal A; Ritchings ... Oncogene. 21 (42): 6488-97. doi:10.1038/sj.onc.1205840. PMID 12226752. Strausberg RL, Feingold EA, Grouse LH, et al. (2003). " ...
Oncogene. 18 (31): 4401-8. doi:10.1038/sj.onc.1202868. PMID 10442630. Induction of Apoptosis (Video). Garland Science / YouTube ...
Oncogene. 19 (6): 745-53. doi:10.1038/sj.onc.1203385. PMID 10698492. Charette SJ, Lavoie JN, Lambert H, Landry J (2000). " ... and transcription factor erythroblastosis virus E26 oncogene homolog 1 (ETS1). In the nucleus, the encoded protein functions as ...
Oncogene. 23 (58): 9314-25. doi:10.1038/sj.onc.1208331. PMID 15602573. "Entrez Gene: WIPI2 WD repeat domain, phosphoinositide ...
1999). "The Bcl-3 oncoprotein acts as a bridging factor between NF-kappaB/Rel and nuclear co-regulators". Oncogene. 18 (22): ... Oncogene. 18 (22): 3316-23. doi:10.1038/sj.onc.1202717. ISSN 0950-9232. PMID 10362352. Rual JF, Venkatesan K, Hao T, et al. ( ...
Oncogene. 31 (18): 2362-72. doi:10.1038/onc.2011.406. PMC 3968770. PMID 21963851. Ji J, Yamashita T, Wang XW (2011). "Wnt/β- ...
Oncogene. 21 (46): 7067-76. doi:10.1038/sj.onc.1205858. PMID 12370829. Scherl A, Couté Y, Déon C, Callé A, Kindbeiter K, ...
Oncogene. England. 21 (11): 1717-26. doi:10.1038/sj.onc.1205229. ISSN 0950-9232. PMID 11896603. Shen, M; Stukenberg P T; ... Oncogene. ENGLAND. 18 (44): 6029-36. doi:10.1038/sj.onc.1202983. ISSN 0950-9232. PMID 10557092. Draetta G, Eckstein J (1997). " ...
The ABL1 proto-oncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell ... "Entrez Gene: ABL1 v-abl Abelson murine leukemia viral oncogene homolog 1". Shah NP, Tran C, Lee FY, Chen P, Norris D, Sawyers ... Shore SK, Tantravahi RV, Reddy EP (December 2002). "Transforming pathways activated by the v-Abl tyrosine kinase". Oncogene. 21 ... Oncogene. 20 (30): 3995-4006. doi:10.1038/sj.onc.1204524. PMID 11494128. Cao C, Leng Y, Huang W, Liu X, Kufe D (October 2003 ...
Oncogene. 22 (12): 1817-21. doi:10.1038/sj.onc.1206283. PMID 12660817. Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete ... Oncogene. 23 (58): 9419-26. doi:10.1038/sj.onc.1208048. PMID 15543234. Andersen JS, Lam YW, Leung AK, et al. (2005). "Nucleolar ... Oncogene. 8 (9): 2537-46. PMID 8395683. Vladimirov SN, Ivanov AV, Karpova GG, et al. (1996). "Characterization of the human ...
Oncogene. 22 (29): 4586-93. doi:10.1038/sj.onc.1206472. PMID 12881716. Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The ...
Oncogene. 18 (22): 3422-6. doi:10.1038/sj.onc.1202691. PMID 10362364. Tanaka K, Hiramoto T, Fukuda T, Miyagawa K (Sep 2000). "A ...
It is published weekly and covers all aspects of the structure and function of Oncogenes. ... Oncogene is one of the world’s leading cancer journals. ... Welcome to Oncogene Publishing the latest research on the ... Join the Oncogene Twitter Community @oncogenejournal. Follow us to keep up-to-date with the latest research and news from ... Oncogene is a Transformative Journal; authors can publish using the traditional publishing route OR via immediate gold Open ...
The performers are oncogenes, the genetic equivalent of reckless acrobats, rampant beasts, and evil clowns. They are given to ... Home Topics Cancer Cancer: A DNA-Ring Circus Where Oncogenes Wreak Havoc ... The paper also presents evidence that oncogenes encoded on ecDNA are among the most highly expressed genes in the transcriptome ... This feature enables tumor cells to generate massive amounts of growth-promoting oncogenes-and evolve more quickly and respond ...
RELA RELA proto-oncogene, NF-kB subunit [Homo sapiens] RELA RELA proto-oncogene, NF-kB subunit [Homo sapiens]. Gene ID:5970 ... RELA proto-oncogene, NF-kB subunitprovided by HGNC. Primary source. HGNC:HGNC:9955 See related. Ensembl:ENSG00000173039 MIM: ... RELA RELA proto-oncogene, NF-kB subunit [ Homo sapiens (human) ] Gene ID: 5970, updated on 24-Sep-2023 ... Knockdown of v-rel reticuloendotheliosis viral oncogene homolog A (RELA) by siRNA inhibits HIV-1 replication in HeLa P4/R5 ...
All the latest news about oncogene from Medical Xpress ... Oncogene. An oncogene is a gene that, when mutated or expressed ... One of the main challenges in oncology is the development of drugs against KRAS oncogenes. These oncogenes-genes that cause ... Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection ... Newly developed drug shows promise against a novel oncogene that supports cancer progression. An enzyme that has been ...
Thus, a product of the mdm-2 oncogene forms a tight complex with the p53 protein, and the mdm-2 oncogene can inhibit p53- ... The mdm-2 oncogene product forms a complex with the p53 protein and inhibits p53-mediated transactivation Cell. 1992 Jun 26;69( ...
Cellular transformation by combined lineage conversion and oncogene expression. View ORCID ProfileBiswajyoti Sahu, View ORCID ... Cellular transformation by combined lineage conversion and oncogene expression Message Subject (Your Name) has forwarded a page ... Here we show that a combination of oncogenes that is characteristic of liver cancer (CTNNB1, TERT, MYC) induces senescence in ... makes them sensitive to transformation by the same oncogenes. The transformed iHeps are highly proliferative, tumorigenic in ...
Boukamp, P.; Stanbridge, E.J.; Cerutti, P.A.; Fusenig, N.E. 1986: The role of the ha ras oncogene in malignant transformation ... Haugen, A.; Ryberg, D.; Hansteen, I.L. 1988: Human epithelial cell carcinogenesis transfection of v ha ras oncogene into nickel ... Malignant transformation of a human fibroblast cell strain by transfection of a v-fes oncogene but not by transfection of a gag ... Malignant transformation of immortalized human skin keratinocytes by ras oncogene transfection. Fusening, N.E.; Boukamp, P.; ...
Proto-oncogene tyrosine-protein kinase lck CD4/CD8 interacting region ... Timeline for Family j.108.1.1: Proto-oncogene tyrosine-protein kinase lck CD4/CD8 interacting region: *Family j.108.1.1: Proto- ... oncogene tyrosine-protein kinase lck CD4/CD8 interacting region first appeared in SCOP 1.67. *Family j.108.1.1: Proto-oncogene ... Proto-oncogene tyrosine-protein kinase lck CD4/CD8 interacting region [103751] (1 species). zinc ion-mediated interaction. ...
"Proto-Oncogene Proteins c-mdm2" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... This graph shows the total number of publications written about "Proto-Oncogene Proteins c-mdm2" by people in this website by ... Below are the most recent publications written about "Proto-Oncogene Proteins c-mdm2" by people in Profiles. ... Mdm2 Phosphorylation Regulates Its Stability and Has Contrasting Effects on Oncogene and Radiation-Induced Tumorigenesis. Cell ...
Start Over You searched for: Format Text ✖ Remove constraint Format: Text Publisher Cold Spring Harbor Laboratory. Press ✖ Remove constraint Publisher: Cold Spring Harbor Laboratory. Press Exhibit Tags oncogenes ✖ Remove constraint Exhibit Tags: oncogenes ...
Proto-oncogene tyrosine-protein kinase Src (human). Find diseases associated with this biological target and compounds tested ...
Moonlight: an approach to identify multiple role of biomarkers as oncogene or tumorsuppressor in different tumor types and ... and oncogenes (OCG). The occurrence of mutations in genes of the first category leads to faster cell proliferation while ... and genes that act as oncogenes (OCGs). This methodology not only allows us to identify genes with dual role (TSG in one cancer ...
Oncogenes, Biomarkers, GFs, CSFs, Hormones, Stains, Lymphokines - 2022 Competitive Shares and Strategies, 2022-2027 Volume and ... Cancer Diagnostic Tests Analyzed in the Report - over 200 current and emerging assays, including Biochemical Markers, Oncogenes ... 2023 Malaysia Tumor Markers Diagnostic Testing Market Assessment - Oncogenes, Biomarkers, GFs, CSFs, Hormones, Stains, ... 2023 Malaysia Tumor Markers Diagnostic Testing Market Assessment - Oncogenes, Biomarkers, GFs, CSFs, Hormones, Stains, ...
"miR-503 represses human cell proliferation and directly targets the oncogene DDHD2 by non-canonical target pairing." BMC ... miR-503 Represses Human Cell Proliferation and Directly Targets the Oncogene DDHD2 by Non-Canonical Target Pairing. ... We identified the proto-oncogene DDHD2 as a target of miR-503 that requires pairing outside of the canonical 5 seed region of ...
Oncogenes. Deoxyribonucleic acid (DNA) probes have found the proto-oncogene C-myc transcription in 75% of AIDS-associated ...
A proto-oncogene normally functions in a way that is similar to a gas pedal - it helps the cell grow and divide. An oncogene ... They are formed by changes or mutations of certain normal genes of the cell called proto-oncogenes. Proto-oncogenes are the ... Oncogenes and tumor suppressor genes. During the 1970s, scientists discovered 2 particularly important families of genes ... Oncogenes: These genes cause cells to grow out of control and become cancer cells. ...
oncogene. Uncovering the Biological Underpinnings of High-Risk Chromosomal Abnormalities in Mutiple Myeloma. * May 28, 2022. . ...
"Oncogene Proteins, Fusion" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular ... Below are the most recent publications written about "Oncogene Proteins, Fusion" by people in Profiles over the past ten years. ... This graph shows the total number of publications written about "Oncogene Proteins, Fusion" by people in UAMS Profiles by year ...
Pim-3 proto-oncogene, serine/threonine kinase - PIM family. Detailed annotation on the structure, function, physiology, ... KID-1/kinase induced by depolarization , kinase induced by depolarization , pim-3 oncogene , Pim-3 proto-oncogene ... Crystal structure of human proto-oncogene serine threonine kinase (PIM1) in complex with a consensus peptide and a beta ... PIM family: Pim-3 proto-oncogene, serine/threonine kinase. Last modified on 06/06/2023. Accessed on 29/09/2023. IUPHAR/BPS ...
"Oncogene Protein tpr-met" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... This graph shows the total number of publications written about "Oncogene Protein tpr-met" by people in this website by year, ... Below are the most recent publications written about "Oncogene Protein tpr-met" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "Oncogene Protein tpr-met". ...
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Proto-Oncogene Protein p21(c-N-ras)*Proto-Oncogene Protein p21(c-N-ras) ... Proto-Oncogene Protein p21(c-Ha-ras)*Proto-Oncogene Protein p21(c-Ha-ras) ... Proto-Oncogene Protein p21(c-Ki-ras)*Proto-Oncogene Protein p21(c-Ki-ras) ... "Proto-Oncogene Proteins p21(ras)" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ...
Proto-Oncogene Protein c-fli-1*Proto-Oncogene Protein c-fli-1 ... Proto-Oncogene Protein c-ets-2. *Proto-Oncogene Protein c-fli-1 ... "Proto-Oncogene Protein c-fli-1" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... This graph shows the total number of publications written about "Proto-Oncogene Protein c-fli-1" by people in this website by ... Below are the most recent publications written about "Proto-Oncogene Protein c-fli-1" by people in Profiles. ...
Sheep anti-Cellular oncogene fos (c-Fos) Polyclonal Antibody (Unconjugated), suitable for WB, IHC-Frozen. ... Product Name Cellular oncogene fos (c-Fos), Sheep Polyclonal Antibody * Product Description google Sheep anti-Cellular oncogene ... Alternative Names c-Fos; Proto-oncogene protein cFOS; cellular oncogene fos; G0/G1 switch regulatory protein 7; FOS; G0S7 ... Alternative Names c-Fos; Proto-oncogene protein cFOS; cellular oncogene fos; G0/G1 switch regulatory protein 7; FOS; G0S7 ...
Because cancer-driven by a single oncogene, such as leukemia driven by the BCR-ABL fusion gene, is amenable to treatment with ... Although two newly described oncogenes known as YAP and TAZ are not generally mutated in human cancers, there is one exception ... Rare-sarcomas; Cancers driven by a single oncogene; Fusion-genes and the mechanism of their activation as fusion proteins, ... EHE - Epithelial Hemangio-Endothelioma, cancer driven by fusions of YAP or TAZ oncogenes with genes that encode transcription ...
5. Analysis of Oncogene Proteins Click on the red plus signs below to view Standard Operating Procedures for each item. ...
2023 Geneseeq Technology Inc. , A Precision Oncology Company. All rights ...
в журнале Oncogene, издательство Nature Publishing Group (United Kingdom), том 39, № 1, с. 1-16 DOI ... в журнале Oncogene, издательство Nature Publishing Group (United Kingdom), том 38, № 25, с. 5091-5106 DOI ... в журнале Oncogene, издательство Nature Publishing Group (United Kingdom), том 37, № 46, с. 6069-6082 DOI ... в журнале Oncogene, издательство Nature Publishing Group (United Kingdom), том 36, № 7, с. 922-932 DOI ...
ddweipdgqitvgqrIgsgsfgtVykgkwhgdvAvkmlnvtaptpqqlqafknEvgvLrktrhvniLlfmgystapqlaivTQWCegsslyhhlhiietkfemiklidiarqtaqgmdyLhaksiiHrdlksnniFlhedltvkIGDFglatvksrwsgshqfeqlsgsilwmapevirmqdknpysfqsdvyafgivlyelmtgqlpysninnrdqiifmvgrgylspdlskvrsncpkamkrlmaeclkkkrderplfpqilasiellarslpk ...
Silencing a metabolic oncogene. / Kim, Jiyeon; DeBerardinis, Ralph J. In: Science, Vol. 340, No. 6132, 2013, p. 558-559.. ... Kim, Jiyeon ; DeBerardinis, Ralph J. / Silencing a metabolic oncogene. In: Science. 2013 ; Vol. 340, No. 6132. pp. 558-559. ... Silencing a metabolic oncogene. Science. 2013;340(6132):558-559. doi: 10.1126/science.1238523 ... title = "Silencing a metabolic oncogene",. abstract = "Small molecules inhibit a mutant enzyme confined to tumors, supporting ...
  • Many cancer drugs target the proteins encoded by oncogenes. (wikipedia.org)
  • Oncogenes play an important role in the regulation or synthesis of proteins linked to tumorigenic cell growth. (wikipedia.org)
  • Proto-oncogenes code for proteins that help to regulate the cell growth and differentiation. (wikipedia.org)
  • Proto-Oncogene Proteins c-mdm2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • This graph shows the total number of publications written about "Proto-Oncogene Proteins c-mdm2" by people in this website by year, and whether "Proto-Oncogene Proteins c-mdm2" was a major or minor topic of these publications. (umassmed.edu)
  • Below are the most recent publications written about "Proto-Oncogene Proteins c-mdm2" by people in Profiles. (umassmed.edu)
  • Below are the most recent publications written about "Oncogene Proteins, Fusion" by people in Profiles over the past ten years. (uams.edu)
  • The GENETIC TRANSLATION product from a GENE FUSION between a sequence from the tpr protein gene on the human CHROMOSOME 1 and the gene for PROTO-ONCOGENE PROTEINS C-MET. (ouhsc.edu)
  • Proto-Oncogene Proteins p21(ras)" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uchicago.edu)
  • Below are the most recent publications written about "Proto-Oncogene Proteins p21(ras)" by people in Profiles. (uchicago.edu)
  • Most oncogenes began as proto-oncogenes: normal genes involved in cell growth and proliferation or inhibition of apoptosis. (wikipedia.org)
  • In 1976, Drs. Dominique Stéhelin [fr], J. Michael Bishop and Harold E. Varmus of the University of California, San Francisco demonstrated that oncogenes were activated proto-oncogenes as is found in many organisms, including humans. (wikipedia.org)
  • Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. (wikipedia.org)
  • In addition, these alterations affect 3 principal categories of genes, as follows: proto-oncogenes, tumor suppressor genes, and DNA repair genes. (medscape.com)
  • This article briefly discusses tumor suppressor genes and then focuses on the role of proto-oncogenes in childhood cancer. (medscape.com)
  • Usually multiple oncogenes, along with mutated apoptotic or tumor suppressor genes will all act in concert to cause cancer. (wikipedia.org)
  • The theory of oncogenes was foreshadowed by the German biologist Theodor Boveri in his 1914 book Zur Frage der Entstehung Maligner Tumoren (Concerning the Origin of Malignant Tumors) in which he predicted the existence of oncogenes (Teilungsfoerdernde Chromosomen) that become amplified (im permanenten Übergewicht) during tumor development. (wikipedia.org)
  • Upon acquiring an activating mutation, a proto-oncogene becomes a tumor-inducing agent, an oncogene. (wikipedia.org)
  • Back in 2014, they discovered that ecDNA plays a central role in the drug resistance of certain brain tumors by enabling tumors to rapidly change the amount of oncogenes they contain-and thereby determine whether a cell transforms into a tumor cell. (genengnews.com)
  • Moonlight: an approach to identify multiple role of biomarkers as oncogene or tumorsuppressor in different tumor types and stages. (bioconductor.org)
  • We then use these scores to predict two specific roles: genes that act as tumor suppressor genes (TSGs) and genes that act as oncogenes (OCGs). (bioconductor.org)
  • Cancer development is influenced by mutations in two distinctly different categories of genes, known as tumor suppressor genes (TSG) and oncogenes (OCG). (bioconductor.org)
  • Here we show that a combination of oncogenes that is characteristic of liver cancer (CTNNB1, TERT, MYC) induces senescence in human fibroblasts and primary hepatocytes. (biorxiv.org)
  • Oncogenes are a physically and functionally diverse set of genes, and as a result, their protein products have pleiotropic effects on a variety of intricate regulatory cascades within the cell. (wikipedia.org)
  • The resultant protein encoded by an oncogene is termed oncoprotein. (wikipedia.org)
  • Thus, a product of the mdm-2 oncogene forms a tight complex with the p53 protein, and the mdm-2 oncogene can inhibit p53-mediated transactivation. (nih.gov)
  • Bishop and Varmus were awarded the Nobel Prize in Physiology or Medicine in 1989 for their discovery of the cellular origin of retroviral oncogenes. (wikipedia.org)
  • Product Description google Sheep anti-Cellular oncogene fos (c-Fos) Polyclonal Antibody (Unconjugated), suitable for WB, IHC-Frozen. (biosensis.com)
  • and the identification of specific activated cellular oncogenes and chromosomal changes in bladder cancer. (cdc.gov)
  • An oncogene is a gene that has the potential to cause cancer. (wikipedia.org)
  • Experiments performed by Dr. G. Steve Martin of the University of California, Berkeley demonstrated that SRC was indeed the gene of the virus that acted as an oncogene upon infection. (wikipedia.org)
  • A proto-oncogene is a normal gene that could become an oncogene due to mutations or increased expression. (wikipedia.org)
  • Another example of an oncogene is the Bcr-Abl gene found on the Philadelphia chromosome, a piece of genetic material seen in Chronic Myelogenous Leukemia caused by the translocation of pieces from chromosomes 9 and 22. (wikipedia.org)
  • Eventually this normal gene mutated into an abnormally functioning oncogene within the Rous sarcoma virus. (wikipedia.org)
  • An oncogene is a gene that, when mutated or expressed at high levels, helps turn a normal cell into a cancer cell. (medicalxpress.com)
  • Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection, to cause cancer. (medicalxpress.com)
  • The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. (uams.edu)
  • Because cancer-driven by a single oncogene, such as leukemia driven by the BCR-ABL fusion gene, is amenable to treatment with inhibitors that target that very single causative agent, there is a lot of interest to develop therapies to treat the EHE. (oist.jp)
  • The first confirmed oncogene was discovered in 1970 and was termed SRC (pronounced "sarc" as it is short for sarcoma). (wikipedia.org)
  • Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead. (wikipedia.org)
  • The authors suggest that ecDNA, because of its increased DNA copy numbers and in association with enhanced chromatin accessibility, promotes massively increased transcription of the oncogenes. (genengnews.com)
  • Furthermore, ecDNA is shown to have a significantly greater number of ultra-long-range interactions with active chromatin, which provides insight into how the structure of circular ecDNA affects oncogene function, and connects ecDNA biology with modern cancer genomics and epigenetics. (genengnews.com)
  • Mdm2 Phosphorylation Regulates Its Stability and Has Contrasting Effects on Oncogene and Radiation-Induced Tumorigenesis. (umassmed.edu)
  • Oncogenes are mutated or amplified forms of genes that in their normal state regulate cell growth. (msdmanuals.com)
  • Dr. Barbacid spent the following months extending his research, eventually discovering that the oncogene was a mutated allele of HRAS and characterizing its activation mechanism. (wikipedia.org)
  • One of the main challenges in oncology is the development of drugs against KRAS oncogenes. (medicalxpress.com)
  • Since the 1970s, dozens of oncogenes have been identified in human cancer. (wikipedia.org)
  • Dr. Robert Weinberg is credited with discovering the first identified human oncogene in a human bladder cancer cell line. (wikipedia.org)
  • Crystal structure of human proto-oncogene serine threonine kinase (PIM1) in complex with a consensus peptide and a beta carboline ligand II. (guidetopharmacology.org)
  • Although two newly described oncogenes known as YAP and TAZ are not generally mutated in human cancers, there is one exception. (oist.jp)
  • A microRNA polycistron as a potential human oncogene. (bvsalud.org)
  • Later on, the term "oncogene" was rediscovered in 1969 by National Cancer Institute scientists George Todaro and Robert Huebner. (wikipedia.org)
  • Once the oncogene is transfected back into a chicken, it can lead to cancer. (wikipedia.org)
  • Some oncogenes inappropriately signal cells to multiply in an uncontrolled manner, leading to a cancer. (msdmanuals.com)
  • SRC was first discovered as an oncogene in a chicken retrovirus. (wikipedia.org)
  • This proto-oncogene may play a role in the regulation of embryonic development and cell growth. (wikipedia.org)
  • Deoxyribonucleic acid (DNA) probes have found the proto-oncogene C- myc transcription in 75% of AIDS-associated lymphomas, which suggests a role for the C- myc oncogene. (medscape.com)
  • The new findings appeared November 20 in Nature , in an article titled, " Circular ecDNA promotes accessible chromatin and high oncogene expression . (genengnews.com)
  • We identified the proto-oncogene DDHD2 as a target of miR-503 that requires pairing outside of the canonical 5' seed region of miR-503, representing a novel mode of miRNA-target pairing. (utexas.edu)
  • More information about the Philadelphia Chromosome below) The proto-oncogene can become an oncogene by a relatively small modification of its original function. (wikipedia.org)
  • Follow us to keep up-to-date with the latest research and news from Oncogene . (nature.com)
  • A proto-oncogene is a normal gene that could become an oncogene due to mutations or increased expression. (wikipedia.org)
  • Upon acquiring an activating mutation, a proto-oncogene becomes a tumor-inducing agent, an oncogene. (wikipedia.org)
  • More information about the Philadelphia Chromosome below) The proto-oncogene can become an oncogene by a relatively small modification of its original function. (wikipedia.org)
  • This proto-oncogene may play a role in the regulation of embryonic development and cell growth. (wikipedia.org)
  • When a proto-oncogene mutates (changes) or there are too many copies of it, it can become turned on (activated) when it is not supposed to be, at which point it's now called an oncogene . (cancer.org)
  • A proto-oncogene normally functions in a way much like the gas pedal on a car. (cancer.org)
  • The present study demonstrated for the first time that neoplastic features of MEC are based on proto-oncogene mutations. (nih.gov)
  • You need info about Human Proto-oncogene serine/threonine-protein kinase pim-1 (PIM1) ELISA Kit or any other Gentaur produtct? (gentaurshop.com)
  • Reversal of aberrant gene expression that is induced by the proto-oncogene c-myc is likely to be effective for treating a variety of tumors that rely on this pathway for growth. (nih.gov)
  • PROJECT SUMMARY/ABSTRACT Environmental genotoxic carcinogens target numerous proto-oncogenes (and tumor-suppressor genes) to induce point mutations in key codons, leading to oncogene activation. (nih.gov)
  • The main mechanisms for activation of proto-oncogenes consist of point mutations, amplifications, and chromosomal translocations. (medscape.com)
  • The current study is skillful to detect of the mutations of the H-RAS oncogene in patient of uterine cancer. (journalcra.com)
  • Activating mutations in the neuroblastoma rat sarcoma viral oncogene homolog (NRAS) gene are common genetic events in malignant melanoma being found in 15C25% of cases. (technologybooksindustrialprojectreports.com)
  • Oncogenic mutations in codons 12, 13, or 61 of the rat sarcoma (RAS) family of small GTPases, Kirsten rat sarcoma viral oncogene homolog (KRAS), Harvey rat sarcoma viral oncogene homolog (HRAS), and neuroblastoma RAS Cd248 viral oncogene homolog (NRAS) occur in approximately one-third of all human cancers with 850173-95-4 supplier NRAS mutations found in about 15C20% of melanomas (1C7). (technologybooksindustrialprojectreports.com)
  • Recently, an oral mitogen activated protein (MAP)/extracellular signal-regulated (ERK) kinase (MEK) inhibitor (MEK162) was tested in patients with metastatic melanoma harboring murine sarcoma viral oncogene homolog B1 (BRAF) or NRAS mutations with encouraging results (12). (technologybooksindustrialprojectreports.com)
  • In a report which 18,191 genes had been sequenced in 11 colorectal tumors, was MM-102 the most regularly mutated oncogene and second and then mutations for all those mutated genes [11]. (cell-signaling-pathways.com)
  • In 1976, Drs. Dominique Stéhelin [fr], J. Michael Bishop and Harold E. Varmus of the University of California, San Francisco demonstrated that oncogenes were activated proto-oncogenes as is found in many organisms, including humans. (wikipedia.org)
  • Although viruses did not cause the tumors, they found that retroviruses containing oncogenes could accelerate tumor growth when injected into mice, and could even induce tumors in normally resistant mice. (nih.gov)
  • The theory of oncogenes was foreshadowed by the German biologist Theodor Boveri in his 1914 book Zur Frage der Entstehung Maligner Tumoren (Concerning the Origin of Malignant Tumors) in which he predicted the existence of oncogenes (Teilungsfoerdernde Chromosomen) that become amplified (im permanenten Übergewicht) during tumor development. (wikipedia.org)
  • Transcription factors, proteins that bind to the regulatory sequences of target genes, compose the largest class of oncogenes identified in pediatric tumors. (medscape.com)
  • Grace Shen-Ong, who worked in Potter's laboratory, and Michael Cole then found that plasma cells that develop tumors have chromosomal translocations involving genes for immunoglobulins and an oncogene called MYC. (nih.gov)
  • And retroviruses had to contain both MYC and another oncogene to induce plasma cell tumors. (nih.gov)
  • Stich M, Ganss L, Puschhof J, Prigge ES, Reuschenbach M, Gutierrez A, Vinokurova S, von Knebel Doeberitz M. 5-aza-2'-deoxycytidine (DAC) treatment downregulates the HPV E6 and E7 oncogene expression and blocks neoplastic growth of HPV-associated cancer cells. (uni-heidelberg.de)
  • Here, we investigated ROS metabolism in primary murine cells following the expression of endogenous oncogenic alleles of Kras, Braf and Myc, and found that ROS are actively suppressed by these oncogenes. (nih.gov)
  • Levels of phospho-ERK, p-MEK phospho-murine thymoma viral oncogene homolog 1 (p-AKT), phospho-S6 ribosomal protein (p-S6), and phosphatase and tensin homolog (PTEN) were measured in 14 main melanomas and 18 metastases from 32 individual specimens of NRAS-mutated melanoma. (technologybooksindustrialprojectreports.com)
  • Bishop and Varmus were awarded the Nobel Prize in Physiology or Medicine in 1989 for their discovery of the cellular origin of retroviral oncogenes. (wikipedia.org)
  • SIRT3 is thus a metabolic non-oncogene addiction and therapeutic target for DLBCLs. (fry-it.com)
  • Oncogenes are activated through well-known chromosomal alterations such as gene fusion, translocation, and focal amplification. (nih.gov)
  • Thirty specimens of blood and tissue were collected for DNA extraction, H-RAS oncogene amplification and histopathology examination. (journalcra.com)
  • Despite much progress in the field, the mechanisms through which oncogenes induce replication stress, particularly in early events leading to carcinogenesis, remains poorly understood. (nih.gov)
  • SRC was first discovered as an oncogene in a chicken retrovirus. (wikipedia.org)
  • Oncogenes and radiation carcinogenesis. (nih.gov)
  • Major gaps in our knowledge of this process include: 1) What are the early steps that contributes to oncogene-induced replication stress in precancerous cells? (nih.gov)
  • Genome-wide sequencing of individual malignancies: mutation may be the predominant oncogene alteration in lung, digestive tract and pancreatic tumor Pancreatic ductal adenocarcinoma (PDAC) may be the most common tumor from the pancreas, composed of over 85% of most situations [4]. (cell-signaling-pathways.com)
  • In a report of 188 main lung adenocarcinomas where 623 genes with known or potential associations to malignancy had been sequenced, was the most regularly mutated oncogene [12]. (cell-signaling-pathways.com)
  • Driver events in pediatric malignancies can occur through loss of function in tumor suppressor genes or gain of function in proto-oncogenes. (medscape.com)
  • Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead. (wikipedia.org)
  • Cite this: Dissecting Oncogenes and Tyrosine Kinases in AML Cells - Medscape - Jul 22, 2003. (medscape.com)
  • Oncogenes can be turned on (activated) in cells in different ways. (cancer.org)
  • Oncogene-induced replication stress is an early driver of genomic instability and is attributed to a plethora of factors, most notably aberrant origin firing, replication-transcription collisions, and defective nucleotide metabolism. (nih.gov)
  • Another example of an oncogene is the Bcr-Abl gene found on the Philadelphia chromosome, a piece of genetic material seen in Chronic Myelogenous Leukemia caused by the translocation of pieces from chromosomes 9 and 22. (wikipedia.org)
  • This approach has been successful in our models of infantile rhabdomyosarcoma and alveolar rhabdomyosarcoma , both driven by respective fusion- oncogenes , VGLL2-NCOA2 and PAX3-FOXO1. (bvsalud.org)
  • Our described zebrafish platform is a rapid method to understand the impact of fusion- oncogene activity, divergent and shared fusion- oncogene biology , and whether any analyzed pathways converge for potential clinically actionable targets. (bvsalud.org)
  • An oncogene is like a gas pedal that is stuck down, which causes the cell to divide out of control. (cancer.org)
  • Proto-oncogenes code for proteins that help to regulate the cell growth and differentiation. (wikipedia.org)