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
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
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
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
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).
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)

c h ras oncogenes, b h ras oncogenes, g h ras oncogenes, f h ras oncogenes, v g ras oncogenes, v b ras oncogenes, v n ras oncogenes, v j ras oncogenes, v u ras oncogenes, v y ras oncogenes, v h eas oncogenes, v h das oncogenes, v h fas oncogenes, v h tas oncogenes, v h 5as oncogenes, v h 4as oncogenes, v h rzs oncogenes, v h rss oncogenes, v h rws oncogenes, v h rqs oncogenes, v h raa oncogenes, v h raz oncogenes, v h rax oncogenes, v h rad oncogenes, v h rae oncogenes, v h raw oncogenes, v h ras incogenes, v h ras kncogenes, v h ras lncogenes, v h ras pncogenes, v h ras 0ncogenes, v h ras 9ncogenes, v h ras obcogenes, v h ras omcogenes, v h ras ojcogenes, v h ras ohcogenes, v h ras onxogenes, v h ras onvogenes, v h ras onfogenes, v h ras ondogenes, v h ras oncigenes, v h ras onckgenes, v h ras onclgenes, v h ras oncpgenes, v h ras onc0genes, v h ras onc9genes, v h ras oncofenes, v h ras oncovenes, v h ras oncobenes, v h ras oncohenes, v h ras oncoyenes, v h ras oncotenes, v h ras oncogwnes, v h ...
TY - JOUR. T1 - Molecular evolutionary rates of oncogenes. AU - Gojobori, Takashi. AU - Yokoyama, Shozo. PY - 1987/11/1. Y1 - 1987/11/1. N2 - Using nine sets of viral and cellular oncogenes, the rates of nucleotide substitutions were computed by using Gojobori and Yokoyamas (1985) method. The results obtained confirmed our previous conclusion that the rates of nucleotide substitution for the viral oncogenes are about a million times higher than those for their cellular counterparts. For cellular oncogenes and most viral oncogenes, however, the rate of synonymous substitution is higher than that of nonsynonymous substitution. Moreover, the pattern of nucleotide substitutions for viral oncogenes is more similar to that for functional genes (such as cellular oncongenes) than for pseudogenes. This implies that nucleotide substitutions in viral oncogenes may be functionally constrained. Thus, our observation supports that nucleotide substitutions for the oncogenes in those DNA and RNA genomes are ...
TY - JOUR. T1 - Pe-1, a novel ets oncogene family member, localizes to chromosome 1q21-q23. AU - Klemsz, Michael. AU - Hromas, Robert. AU - Raskind, Wendy. AU - Bruno, Edward. AU - Hoffman, Ronald. PY - 1994/3/15. Y1 - 1994/3/15. N2 - The v-ets\ oncogene family shares a conserved peptide motif called the ETS domain that mediates sequence-specific DNA binding. This motif is unique among transcription factor families. Using partially degenerate oligonucleotides from conserved regions of the ETS domain and the polymerase chain reaction, we isolated a new member of the v-ets family designated PE-1 from HL60 cells. PE-1 was expressed as an approximately 7.5-kb transcript in most cell lines tested. In the hairy cell leukemia line Eskol, there was an additional 1.8-kb transcript observed. PE-1 was the most common ETS domain gene found in CD34+HLA-DR- hematopoietic progenitors. PE-1 was localized to human chromosome 1q21-q23 using both in situ chromosomal hybridization and human-hamster hybrids.. AB - ...
TY - JOUR. T1 - Identification of 33 candidate oncogenes by screening for base-specific mutations. AU - Tuupanen, S.. AU - Hanninen, U. A.. AU - Kondelin, J.. AU - von Nandelstadh, P.. AU - Cajuso, Tatiana. AU - Gylfe, A. E.. AU - Katainen, Riku. AU - Tanskanen, T.. AU - Ristolainen, H.. AU - Bohm, J.. AU - Mecklin, J-P. AU - Järvinen, Heikki. AU - Renkonen-Sinisalo, L.. AU - Andersen, C. L.. AU - Taipale, M.. AU - Taipale, Jussi. AU - Vahteristo, P.. AU - Lehti, K.. AU - Pitkanen, E.. AU - Aaltonen, L. A.. PY - 2014/10/14. Y1 - 2014/10/14. KW - oncogene. KW - mutation hotspot. KW - microsatellite instability. KW - colorectal cancer. KW - exome sequencing. KW - NONPOLYPOSIS COLORECTAL-CANCER. KW - BLOCKADE. KW - GENES. KW - 3122 Cancers. U2 - 10.1038/bjc.2014.429. DO - 10.1038/bjc.2014.429. M3 - Article. VL - 111. SP - 1657. EP - 1662. JO - British Journal of Cancer. JF - British Journal of Cancer. SN - 0007-0920. IS - 8. ER - ...
GeneQuery™ Human Oncogenes qPCR Array Kit ...
Cancers can exhibit marked tumor regression after oncogene inhibition through a phenomenon called oncogene addiction. The ability to predict when a tumor will exhibit oncogene addiction would be useful in the development of targeted therapeutics. Oncogene addiction is likely the consequence of many cellular programs. However, we reasoned that many of these inputs may converge on aggregate survival and death signals. To test this, we examined conditional transgenic models of K-rasG12D- or MYC-induced lung tumors and lymphoma combined with quantitative imaging and an in situ analysis of biomarkers of proliferation and apoptotic signaling. We then used computational modeling based on ordinary differential equations (ODEs) to show that oncogene addiction could be modeled as differential changes in survival and death intracellular signals. Our mathematical model could be generalized to different imaging methods (computed tomography and bioluminescence imaging), different oncogenes (K-rasG12D and ...
TY - JOUR. T1 - The PU.1 transcription factor is the product of the putative oncogene Spi-1. AU - Goebl, Mark G.. PY - 1990/6/29. Y1 - 1990/6/29. UR - UR - U2 - 10.1016/0092-8674(90)90676-6. DO - 10.1016/0092-8674(90)90676-6. M3 - Letter. C2 - 2364426. AN - SCOPUS:0025283714. VL - 61. SP - 1165. EP - 1166. JO - Cell. JF - Cell. SN - 0092-8674. IS - 7. ER - ...
DNA is often called the molecule of life. Small coding sequences along a strand of DNA are called genes. Genes control all the functions of the body. While all the genes a person will ever need are present in all cells, they are not all active at the same time. Genes that control growth and development, for instance, are active only at certain times of life. The rest of the time they are inactive. Inactive genes are part of the human genetic make-up. Sometimes, however, a gene that controls growth and should be inactive is stimulated to do its work. If the work is done at an inappropriate time, cells multiply at random and a cancer may develop. The inactive gene is called a proto-oncogene. When it is activated it is called an oncogene. Oncogenes act by producing normal signals at the wrong time. Oncogenes may work alone or together with other oncogenes. Some oncogenes act early in the process of tumor formation. Others act later. Some are initiators, which start the process, and others are ...
RAB6B Human - Recombinant Human RAB6B, Member RAS Oncogene Family (5ug) - Read User Reviews, Features, Research Applications and get the Best Price/Quote
Buy RAB39 elisa kit, Mouse RAB39, member RAS oncogene family ELISA Kit-NP_780771.1 (MBS9340534) product datasheet at MyBioSource, ELISA Kits
Alterations involving the ROS (v-ros UR2 sarcoma virus oncogene homolog 1) gene such as mutations, overexpression and gene rearrangements has been implicated in carcinogenesis and has been demonstrated to be a relevant target for ALK inhibitors. While emerging reports have demonstrated the role of ROS rearrangement in non-small cell lung cancer and cholangiocarcinoma, the functional significance of ROS dysregulation in solid tumors remain largely unstudied. The investigators aims are: (1) To characterize the frequency of ROS gene fusion, ROS protein overexpression and ROS gene mutations in cell lines and tumors from patients with hepatocellular carcinoma, colorectal, gastric, breast, ovarian, cholangiocarcinoma and non-small cell lung cancer, (2) To identify novel ROS gene variants in human solid tumors harboring ROS aberrations using next generation sequencing (NGS), (3) To determine the functional relevance of novel ROS gene variants identified with NGS, (4) To characterize the sensitivity of ...
The oncogenic BCR-ABL kinase of chronic myelogenous leukemia (CML) helped define the paradigm for oncogene addiction. Block the mutant kinase in cancer cells, and you break their signaling habit. Using tyrosine kinase inhibitors, clinicians have been able to achieve control of CML, and this approach has been successfully applied to other cancers-BRAF mutant melanoma, for example. Now, Asmussen et al. explore the nature of oncogene addition in CML and describe a negative feedback loop that may explain why these cells cant easily kick the BCR-ABL habit.. The authors began with the observation that transient exposure to tyrosine kinase inhibitors commits CML cells to apoptosis, suggesting a durable alteration in protein signaling that persists even after the drug wears off. Beginning with an unbiased screen of altered phophoproteins, the authors found that growth factor (GF) signaling is key to this process. They then made use of the human erytholeukemia cell line TF1, which can be rendered ...
Fingerprint Dive into the research topics of Oncogenic shock: Explaining oncogene addiction through differential signal attenuation. Together they form a unique fingerprint. ...
Understanding the genetic mechanisms which underlie tumor development will provide a foundation for developing new generations of better and more effective cancer therapies. To address this fundamental issue, new technologies are needed that are superior to those currently available. Current state of the art mouse models enable testing the stochastic activation of oncogenes in a cell type specific fashion and provide a mechanism for testing targeted therapies. Despite these desirable features, their limited accessibility and feasibility precludes their implementation in most laboratories. Moreover, as the list of oncogenes continues to grow, reliable and efficient technologies are needed that can assess several oncogenes simultaneously in order to facilitate rapid analysis of tumorigenicity and their responses to therapy. This application provides a solution to all these issues by developing an innovative transgenic mouse platform (Crainbow) to rapidly, efficiently, and cost effectively create ...
Cancer is caused by an accumulation of genetic alterations that confer a survival advantage to the neoplastic cell. J. L. Jameson(p73) Oncogenes are [g]enes that normally play a role in growth but, when overexpressed or mutated, can foster the growth of cancer. Oncogenes were discovered and characterized in viruses and animal experimental systems. These genes exist widely outside the systems in which they were discovered, and their normal cellular homologues are important in cell division and differentiation. Human oncogenes should be expressed according to style for human gene symbols (see , Human Gene Nomenclature). Mouse oncogenes (and other nonhuman oncogenes) should Less ...
Cancer is caused by an accumulation of genetic alterations that confer a survival advantage to the neoplastic cell. J. L. Jameson(p73) Oncogenes are [g]enes that normally play a role in growth but, when overexpressed or mutated, can foster the growth of cancer. Oncogenes were discovered and characterized in viruses and animal experimental systems. These genes exist widely outside the systems in which they were discovered, and their normal cellular homologues are important in cell division and differentiation. Human oncogenes should be expressed according to style for human gene symbols (see , Human Gene Nomenclature). Mouse oncogenes (and other nonhuman oncogenes) should Less ...
Hypomethylation of ras oncogenes in primary human cancers.: We have examined the methylation status of two cellular oncogenes, c-Ha-ras and c-Ki-ras, in primary
Many theories of neoplasia suggest that oncogenic transformations result from aberrations in the control mechanisms which normally regulate growth and differentiation during embryonic development. It has recently become clear that many proto-oncogenes are differentially expressed during embryonic development and may thus be important embryonic regulatory molecules. We report here that the products of two transforming oncogenes int-2 and hst/ks (now called kfgf) can, with different potencies, induce mesoderm formation in isolated Xenopus laevis animal pole explants and stimulate DNA synthesis in mammalian fibroblasts. The results suggest that these proteins may function as mesoderm inducers in mammalian embryogenesis and that similar receptor/signalling pathways may be utilized for developmental and oncogenic processes. Finally, we have shown that the Xenopus assay system used in this study provides a powerful screen for protein factors that are active in development. ...
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are often mutated or expressed at high levels. Most normal cells will undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered and malfunctioning. Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead. Most oncogenes began as proto-oncogenes, normal genes involved in cell growth and proliferation or inhibition of apoptosis. If normal genes promoting cellular growth, through mutation, are up-regulated, (gain of function mutation) they will predispose the cell to cancer and are thus termed oncogenes. Usually multiple oncogenes, along with mutated apoptotic or tumor suppressor genes will all act in concert to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the proteins encoded by oncogenes.
In cancer cells associated with human papillomavirus (HPV) infections, the viral genome is very often found integrated into the cellular genome. The viral oncogenes E6 and E7 are transcribed from the viral promoter, and integration events that alter transcriptional regulation of this promoter contribute to carcinogenic progression. In this study, we detected highly enriched binding of the super-enhancer markers Brd4, MED1, and H3K27ac, visible as a prominent nuclear focus by immunofluorescence, at the tandemly integrated copies of HPV16 in cells of the cervical neoplasia cell line W12 subclone 20861. Tumor cells are often addicted to super-enhancer-driven oncogenes and are particularly sensitive to disruption of transcription factor binding to the enhancers. Treatment of 20861 cells with bromodomain inhibitors displaced Brd4 from the HPV integration site, greatly decreased E6/E7 transcription, and inhibited cellular proliferation. Thus, Brd4 activates viral transcription at this integration ...
TY - JOUR. T1 - Functional oncogene signatures guide rationally designed combination therapies to synergistically induce breast cancer cell death. AU - Guest, Stephen T.. AU - Kratche, Zachary R.. AU - Irish, Jonathan C.. AU - Wilson, Robert C.. AU - Haddad, Ramsi. AU - Gray, Joe W.. AU - Garrett-Mayer, Elizabeth. AU - Ethier, Stephen P.. PY - 2016. Y1 - 2016. N2 - A critical first step in the personalized approach to cancer treatment is the identification of activated oncogenes that drive each tumor. The Identification of driver oncogenes on a patient-by-patient basis is complicated by the complexity of the cancer genome and the fact that a particular genetic alteration may serve as a driver event only in a subset of tumors that harbor it. In this study, we set out to identify the complete set of functional oncogenes in a small panel of breast cancer cell lines. The cell lines in this panel were chosen because they each contain a known receptor tyrosine kinase (RTK) oncogene. To identify ...
Gene rearrangements ALK and ROS1 that are known to drive subsets of lung cancer are also present in colorectal cancer according to a recent study in Molecular Cancer Research.
How is growth controlled in normal cells? How are the growth control mechanisms perturbed in cancer cells? This book provides an up-to-date description of research aimed at resolving these questions. It is organized into four sections, each containing a series of short reviews written by experts in the field. The general headings are: growth factors, receptors, and related oncogenes: transduction of mitogenic signals and ras oncogenes; nuclear oncogenes and regulation of gene expression; and multiple steps involved in malignant transformation. The articles emphasize concepts rather than detailed facts and are intended not only for specialists in the field but also for interested readers, such as physicians and advanced students, who wish to stay abreast of developments in one of the most exciting fields in current biomedical research.
Functional enhancers can accompany oncogenes on the circularized extrachromosomal amplicons found in glioma and other tumors, enhancing cancer growth.
Another version of this view is that cancer cells have altered developmental states. In normal development, cells start out pluripotent, when they are proliferative but not very differentiated, and they eventually become less proliferative as they become more differentiated. Some of the more aggressive cancers involve a reversion to the more proliferative, less differentiated state. But they are not totally undifferentiated, and often you can see signs of them sort of trying to form the original organ if you look within the tumor.. An example of the molecular differences in cancer is the very different prognosis depending on the particular driver mutation present in leukemia. As of a few years ago, a patient with a translocation between chromosomes 12 and 21 resulting in a TEL/AML1 fusion protein would have acyte myeloid leukemia (AML), with a 90% survival rate. A patient with a translocation between chromosomes 9 and 22 (Philadelphia chromosome) resulting in an BCR/ABL fusion protein would ...
This gene is a member of the Rab family of small G proteins and plays a role in regulating membrane trafficking between trans-Golgi network (TGN) and recycling endosomes (RE). The encoded protein is involved in the assembly of tight junctions, which are components of the apical junctional complex (AJC) of epithelial cells. The AJC plays a role in forming a barrier between luminal contents and the underlying tissue. Additional functions associated with the protein include endocytic recycling of occludin, regulation of epithelial cell scattering, neuronal regeneration and regulation of neurite outgrowth. Alternately spliced transcript variants have been observed for this gene. A pseudogene associated with this gene is located on chromosome 12. [provided by RefSeq, Jan 2013 ...
RAB31 Human Recombinant produced in E.Coli is a single, non-glycosylated polypeptide chain containing 232 amino acids (1-195 a.a) and having a molecular mass of 25.9kDa.RAB31 is fused to a 37 amino acid His-tag at N-terminus & purified by proprietary chromatographic techniques.
RAB13 Human Recombinant produced in E.coli is a single, non-glycosylated polypeptide chain containing 220 amino acids (1-200) and having a molecular mass of 24.7 kDa.The RAB13 is fused to a 20 amino acid His-Tag at N-terminus and purified by proprietary chromatographic techniques.
The KOMP Repository is located at the University of California Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...
Cancer is a genetic disease that evolves over years with accumulating genetic and epigenetic abnormalities that confer an enhanced capacity to proliferate and evade apoptosis, eventually compromising the host (1, 2). Although cancer exhibits complex genetic aberrations and functional deregulations, it has been shown that abrogation of certain apical oncogenes can effectively inhibit cancer cell growth and prolong patient survival-a phenomenon termed oncogene addiction (3). In accordance with this concept, molecularly targeted drugs have been developed and successfully used in treating cancer patients, exemplified by the use of imatinib for chronic myelogenous leukemia, erlotinib for lung cancer, and sunitinib for kidney cancer (4). Despite these recent strides against cancer, most end-stage cancer patients still succumb to their diseases, highlighting the urgent need for novel anticancer therapeutic strategies. Recently, the non-oncogene addiction hypothesis was proposed based on the heavy ...
References. Calabretta B, Kaczmarek LL, Selleri L, Torelli G, Ming PML, Ming SC and Mercer WE (1986) Growth-dependent expression of human Mr 53,000 tumor antigen messenger RNA in normal and neoplastic cells. Cancer. Res. 46: 5738-5742.. Deppert W, Buschhausendenker G, Patschinsky T and Steinmeyer K (1990) Cell cycle control of p53 in normal (3T3) and chemically transformed (Meth-A) mouse cells . II. requirement for cell cycle progression. Oncogene 5: 1701-1706.. Eliyahu D, Raz A, Gruss P, Givol D and Oren M (1984) Participation of p53 cellular tumour antigen in transformation of normal embryonic cells. Nature 312: 646-649.. Jenkins JR, Rudge K, Chumakov P and Currie GA (1985) The cellular oncogene p53 can be activated by mutagenesis. Nature 317: 816-818.. Jenkins JR, Rudge K and Currie GA (1984) Cellular immortalization by a cDNA clone encoding the transformation-associated phosphoprotein p53. Nature 312: 651-654.. Mercer WE, Avignolo C and Baserga R (1984) Role of the p53 protein in cell ...
miRNAs modulate gene expression programs to control cellular processes. Analyses of bulk tissue from epithelial cancers have indicated that the levels of miR-143 and miR-145, two miRNAs shown to repress the expression of several oncogenes, are decreased compared to adjacent normal tissue, suggesting a tumor-suppressive role. In contrast, in normal tissues, the miR-143/145 cluster is expressed in the stroma and promotes epithelial growth during injury responses. To clarify the role of miR-143/145 in tumorigenesis and to elucidate the cell-type specificity of miR-143/145 expression in cancer, Dimitrova, Gocheva, and colleagues evaluated an autochthonous mouse model of Kras-mutant/Trp53-null (KP)-driven lung adenocarcinomas. Tumor-specific deletion or induced overexpression of miR-143/145 in KP mice did not affect tumor development or overall survival; however, organism-wide loss of miR-143/145 in vivo resulted in decreased lung tumor burden, suggesting that stromal miR-143/145 supports lung tumor ...
Gene in a virus that is able to produce a malignant change in an infected cell; several have been identified in human tissue as potential causes of cancer. Researchers are attempting to isolate anti-oncogenes that suppress tumours and may be used in the treatment of cancer. Certain oncogenes may play a role in normal growth and development; if they are damaged or mutated, cancer may result ...
In virtually all epithelial tumors, growth factor receptor activity is deregulated by activated mutations, genomic amplification, and autocrine loops. The dependence of tumor cell survival upon the driving oncogene has been called oncogene addiction and demonstrates the acute sensitivity of cancer cells to inhibition of the pathways driving their proliferation, growth and survival. Major questions regarding the sensitivity of solid tumors to targeted kinase inhibitors is why some tumors respond and others do not and why ones which respond still are able to develop resistance through the activation of other pathways. Robust, but not durable, response to receptor tyrosine kinase inhibitors (RTKIs) highlights the need to inhibit pathway activity at multiple levels.. In this study, we identify extensive signaling networks downstream of receptor tyroine kinases (RTKs) across multiple spaces, including phosphorylation, acetylation, and methylation. We used the established method of TMT labeling ...
Some tumors addiction to the over-expression of a single oncogene provides a weakness for a molecularly targeted therapy to exploit. A number of targeted
pep:known chromosome:VEGA66:5:115631908:115647736:1 gene:OTTMUSG00000014704 transcript:OTTMUST00000034877 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Rab35 description:RAB35 member RAS oncogene family ...
RAB17 antibody [4E7] (RAB17, member RAS oncogene family) for ICC/IF, IHC-P, WB. Anti-RAB17 mAb (GTX83739) is tested in Human samples. 100% Ab-Assurance.
RAB4A antibody [4E11] (RAB4A, member RAS oncogene family) for ELISA, FACS, IHC-P, WB. Anti-RAB4A mAb (GTX60601) is tested in Human, Mouse, Monkey samples. 100% Ab-Assurance.
The product of both the viral and cellular myc genes has been implicated as being a primary mediator of events leading to cellular transformation. In addition,...
Some normal genes may be transformed into genes that promote the growth of cancer. Its presence may give us information about how likely it is that a cancer will spread.
Looking for online definition of cellular oncogene c-fos in the Medical Dictionary? cellular oncogene c-fos explanation free. What is cellular oncogene c-fos? Meaning of cellular oncogene c-fos medical term. What does cellular oncogene c-fos mean?
Looking for online definition of RAB41, member RAS oncogene family in the Medical Dictionary? RAB41, member RAS oncogene family explanation free. What is RAB41, member RAS oncogene family? Meaning of RAB41, member RAS oncogene family medical term. What does RAB41, member RAS oncogene family mean?
The effects of viral or activated cellular oncogenes on sensitivity to γ rays, ultraviolet light, and heat shock were examined in SHOK (Syrian hamster Osaka-Kanazawa) cells and their transfectants. Resistance to γ rays was conferred by the introduction of v-mos or c-cot genes, which coded serine/threonine kinase. Cells transfected with v-mos and c-cot genes increased their resistance to ultraviolet light and heat shock compared to their parent cells (SHOK cells). Of the activated ras genes, the N-ras gene developed a SHOK cell phenotype resistant to γ rays and ultraviolet light. The Ha-ras gene produced SHOK cells resistant to ultraviolet light and heat shock, while introduction of the Ki-ras gene did not affect sensitivity. The v-erbB gene was found to be involved in the development of resistance to heat shock. Transfection with neo, c-myc, and v-fgr genes had little or no effect on cell survival. The karyotypes of SHOK cells and oncogene-containing cells were compared. No alterations were ...
TY - JOUR. T1 - Synthesis and Evaluation of Multisubstrate Inhibitors of an Oncogene-Encoded Tyrosine-Specific Protein Kinase.. AU - Kruse, Carolyn H.. AU - Holden, Kenneth G.. AU - Lynn Pritchard, M.. AU - Feild, John A.. AU - Rieman, David J.. AU - Greig, Russell G.. AU - Poste, George. PY - 1988/9/1. Y1 - 1988/9/1. N2 - The synthesis and testing of potential multisubstrate inhibitors of tyrosine-specific protein kinases are described. One of the substrates, ATP, was mimicked by the known kinase inhibitor 5′-[4-(fluorosulfonyl)benzoyl]adenosine, which was covalently linked via the sulfonyl moiety to tyrosine mimics. The resulting multisubstrate inhibitors were tested for their ability to inhibit the transfer of phosphate from ATP to a protein acceptor by p60v-abl the tyrosine kinase encoded by the transforming gene (v-abl) of the Abelson murine leukemia virus (A-MuLV). Although the series of inhibitors displayed moderately potent activity (IC50 values as low as 19 μM), the absence of large ...
Acquisition of genes via horizontal transfer rather than by inheritance is frequently observed in bacteria. Now, Swedish researchers demonstrate that a similar phenomenon can occur between eucaryotic cells. Oncogenes from a dying cell can be transferred to a nearby cell via phagocytosis, a process through which one cell engulfs another. If the recipient cell is already genetically unstable, the newly acquired oncogenes can lead to tumor formation.. The researchers propose that this horizontal transfer of genes could be one route by which cells accumulate genetic abnormalities. The study also indicates that even after a cell dies, its genetic material entire chromosomes in some cases can be rescued by other cells.. The scientists mixed dying rat cells carrying cancer-causing oncogenes with mouse cells lacking p53, a tumor-suppressing gene. The p53-deficient cells developed tumor-like characteristics. The same experiment was done with mouse cells carrying p53. In contrast, however, the rat cells ...
Published 6 March 2018. The PI3K/Akt signaling pathway, Notch, and other oncogenes cooperate in the induction of aggressive cancers. Elucidating how the PI3K/Akt pathway facilitates tumorigenesis by other oncogenes may offer opportunities to develop drugs with fewer side effects than those currently available. Here, using an unbiased in vivo chemical genetic screen in Drosophila, we identified compounds that inhibit the activity of proinflammatory enzymes nitric oxide synthase (NOS) and lipoxygenase (LOX) as selective suppressors of Notch-PI3K/Akt cooperative oncogenesis. Tumor silencing of NOS and LOX signaling mirrored the antitumor effect of the hit compounds, demonstrating their participation in Notch-PI3K/Akt-induced tumorigenesis. Oncogenic PI3K/Akt signaling triggered inflammation and immunosuppression via aberrant NOS expression. Accordingly, activated Notch tumorigenesis was fueled by hampering the immune response or by NOS overexpression to mimic a protumorigenic environment. Our lead ...
Cancer cells escape normal growth control mechanisms as a consequence of activating (i.e., gain-of-function) mutations and/or increased expression of one or more cellular protooncogenes and/or inactivating (i.e., loss-of function) mutations and/or decreased expression of one or more tumor suppressor genes. Most oncogene and tumor suppressor gene products are components of signal transduction pathways that control cell cycle entry or exit, promote differentiation, sense DNA damage and initiate repair mechanisms, and/or regulate cell death programs. Several oncogenes and tumor suppressor genes belong to the same signaling pathway. Perhaps the best-characterized pathway includes D-type cyclin/cdk complexes, which can be oncogenes, and two tumor suppressor genes, the p16 cyclin/cdk inhibitor and the retinoblastoma gene product (reviewed in ref. 1). Nearly all tumors have mutations in multiple oncogenes and tumor suppressor genes, indicating that cells employ multiple parallel mechanisms to regulate ...
Inflammation plays an intrinsic component in tumor initiation. oncogene irritation and activation in gastrointestinal tumors such as for example colorectal hepatic and pancreatic tumors. STAT3 and nf-κb will be the two most common pathways that are deregulated via these oncogenes. Understanding these connections might produce effective therapeutic approaches for tumor treatment and prevention. INTRODUCTION Oncogenes are fundamental motorists of tumorigenesis with irritation promoting many areas of tumor advancement such as for example initiation development and metastasis. Although some authors have talked about the need for inflammation of these processes the result of oncogene activation on irritation is Dorzolamide HCL only lately getting to be unraveled (1-3). Within this review we discuss the most recent advances in identifying how Dorzolamide HCL oncogenes or microRNAs (miRNAs) maintain and gasoline irritation which promotes oncogene-mediated tumor development within an organ-specific ...
Oncogenes and anti-oncogenes form two families of genes. If abnormal both may induce malignancies. They are distinguished, however, by two components. Oncogenes play a certain role in a given period of development (mainly during organogenesis). As soon as function has been completed they are inactivated. Aberrant reactivation even of one allele may induce tumors in different tissues independent of age. Anti-oncogenes on the other hand protect the organism, functioning mainly at the level of cell cycle regulation. Because one allele is sufficient for sustaining of adequate function both alleles of the anti-oncogene must be destroyed before tumor development is possible. Such a tumor will be tissue- and age-specific.
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How might this happen? Several potential regulatory schemes could contribute to the differential decay of prosurvival and proapoptotic signals on oncogene inactivation. For example, it is well documented in numerous cell culture studies that acute inactivation of various oncoproteins leads to the rapid dephosphorylation (and inactivation) of AKT, which is both a key cell survival mediator in tumor cells and a downstream target of many of the common oncoproteins (e.g., tyrosine kinases such as EGFR and Src). Although the molecular pathways that link these active kinases to an apoptotic response are poorly understood, these pathways are likely to involve a cascade of signaling events, some of which culminate in gene expression changes. Inactivation of an upstream kinase may not be sensed by downstream proapoptotic mediators for a longer period of time than that required for AKT inactivation, thereby creating a signaling imbalance that leads to an irreversible apoptotic response. Certainly, ...
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The tumor suppressor gene MEN1 and several oncogenes including CCND1/cyclin D1/PRAD1 map to chromosome 11q13. However, molecular and cytogenetic analysis suggests the presence of a second tumor suppressor locus at this chromosome region. We have identified a novel gene from chromosome 11q13, which e …
Researchers at the University of Texas M. D. Anderson Cancer Center report they have discovered a potential oncogene in ovarian cancer, which is the leading cause of gynaecological cancer death in U.S. women.
You searched for: Exhibit Tags oncogenes Remove constraint Exhibit Tags: oncogenes Genre Charts (graphic documents) Remove constraint Genre: Charts (graphic documents) Language English Remove constraint Language: English ...
Maestro, R., Dei Tos, A. P., Hamamori, Y., Krasnokutsky, S., Sartorelli, V., Kedes, L., Doglioni, C., Beach, D. H., Hannon, G. J. (1999) Twist is a potential oncogene that inhibits apoptosis. Genes and Development, 13 (17). pp. 2207-17. ISSN 0890-9369 Martienssen, R. (1996) Epigenetic phenomena: Paramutation and gene silencing in plants. Current Biology, 6 (7). pp. 810-813. ISSN 0960-9822 Martienssen, R., Lippman, Z., May, B., Ronemus, M., Vaughn, M. (2004) Transposons, tandem repeats, and the silencing of imprinted genes. Cold Spring Harbor symposia on quantitative biology, 69. pp. 371-9. ISSN 0091-7451 (Print)0091-7451 (Linking) Matapurkar, A., Lazebnik, Y. (2006) Requirement of cytochrome c for apoptosis in human cells. Cell Death Differ, 13 (12). pp. 2062-7. ISSN 1350-9047 (Print) McCaffrey, A. P., Meuse, L., Pham, T. T. T., Conklin, D. S., Hannon, G. J., Kay, M. A. (2002) Gene expression - RNA interference in adult mice. Nature, 418 (6893). pp. 38-39. ISSN 0028-0836 Mittal, V. (2004) ...
Oncogene-encoded proteins c-Myc, n-Myc, and l-Myc function in cell proliferation, differentation and neoplastic disease. A mutated version of Myc is found in many cancers, which causes Myc to be constitutively expressed. This leads to the unregulated expression of many genes, some of which are involved in cell proliferation, and result in the formation of cancer. c-Myc is a transcription factor and is a proto-oncogene that is the focal point in cell cycle regulation, metabolism, apoptosis, differentiation, cell adhesion, and tumorigenesis. A common human translocation involving Myc is t(8;14), which is criticial to the development of most cases of Burkitts Lymphoma. Malfunctions in Myc have also been found in carcinoma of the cervix, colon, breast, lung, and stomach ...
Thomas has had an exceptionally prolific and diverse career, making fundamental discoveries on human leukemia viruses, co-discovering the first human oncogenes, and revealing molecular regulatory mechanisms of cellular differentiation ad reprogramming. [more] ...
View Notes - Lecture 29 Oncogenes and Tumor Suppressors from PHARM HB at UCSD. Recognize that most cancers originate in tissues and cell types that undergo continuous regeneration Explain the
Cancer is a leading cause of mortality in the world today. Mutation in the K-ras oncogene is common in most human cancers. K-ras oncogene expression was specifically downregulated by 58.7% by K-ras silencing siRNA, and ...
Charles Sawyers, who began his research career just as the genetic details of human oncogenes were emerging, codeveloped Gleevec, the quintessential targeted cancer therapy.. 0 Comments. ...
Charles Sawyers, who began his research career just as the genetic details of human oncogenes were emerging, codeveloped Gleevec, the quintessential targeted cancer therapy.. 0 Comments. ...
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Protein syn cael ei godio yn y corff dynol gan y genyn RAB6B yw RAB6B a elwir hefyd yn Ras-related protein Rab-6B a RAB6B, member RAS oncogene family (Saesneg). Segment o DNA ywr genyn, syn amgodio ffwythiant arbennig. Maer genyn yma wedi ei leoli ar yr edefyn ôl o gromosom dynol 3, band 3q22.1.[2] ...
Complete information for RAB40B gene (Protein Coding), RAB40B, Member RAS Oncogene Family, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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pep:known chromosome:VEGA66:10:93247414:93311135:-1 gene:OTTMUSG00000033471 transcript:OTTMUST00000084101 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Elk3 description:ELK3, member of ETS oncogene family ...
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Mutation or inactivation of RB occurs in most human tumors and results in the deregulation of several E2F family transcription factors. Among the E2F family, E2F3 has been implicated as a key regulator of cell proliferation ...
In the previous two parts Ive described how cell biologists (and scientists in related fields) began to uncover the causes of cancer. Today Ill wrap things up with a recent discovery that goes full circle. But first lets have a recap and an expansion on some key points.
MN1, MGCR, MGCR1, MGCR1-PEN, dJ353E16.2, meningioma (disrupted in balanced translocation) 1, MN1 proto-oncogene, ...
"Oncogene. 27 (34): 4702-11. doi:10.1038/onc.2008.109. PMC 2748240. PMID 18408761.. ...
Oncogene. 2002 October 21;21(48):7435-51. *^ Jiang, Hao; Gelhaus, Stacy L.; Mangal, Dipti; Harvey, Ronald G.; Blair, Ian A.; ...
"Specific activation of microRNA-127 with downregulation of the proto-oncogene BCL6 by chromatin-modifying drugs in human cancer ...
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Li J, Witte DP, Van Dyke T, Askew DS (April 1997). "Expression of the putative proto-oncogene His-1 in normal and neoplastic ... Further analysis of one ultraconserved ncRNA suggested it behaved like an oncogene by mitigating apoptosis and subsequently ... Oncogene. 23 (39): 6684-92. doi:10.1038/sj.onc.1207880. PMID 15221013. Eis PS, Tam W, Sun L, et al. (March 2005). "Accumulation ... Oncogene. 26 (6): 851-8. doi:10.1038/sj.onc.1209846. PMID 16878148. Reis EM, Nakaya HI, Louro R, et al. (August 2004). " ...
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Sattler, Martin; James D. Griffin (April 2001). "Mechanisms of transformation by the BCR/ABL oncogene". International Journal ... Nimmanapalli, R.; Bhalla, K. (2002). "Novel targeted therapies for Bcr-Abl positive acute leukemias: Beyond STI571". Oncogene. ...
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Chromosom DNA cancer cell gene genes immunodeficiency leukemia molecular biology mutation oncogene tumor ...
It is published weekly and covers all aspects of the structure and function of Oncogenes. ... Oncogene is one of the worlds 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 ... A sincere thank you to all of the reviewers listed here, who took the time to review for Oncogene in 2020. The journal could ...
Oncogenes and cancer.. Croce CM1.. Author information. 1. Department of Molecular Virology, Immunology, and Medical Genetics ...
Original citation: J. Clin. Invest.114:1362 (2004).. Citation for this erratum: J. Clin. Invest.114:1820 (2004).. The name "Lewis Chodosh" was spelled incorrectly as "Lou Chodash." We regret this error.. ...
"Oncogene. 8 (11): 2925-2929. PMID 8414495.. *^ Baloh RH, Enomoto H, Johnson EM, et al. (2000). "The GDNF family ligands and ... The RET proto-oncogene encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor (GDNF ... 1993). "Exon structure and flanking intronic sequences of the human RET proto-oncogene". Biochem. Biophys. Res. Commun. 196 (3 ... ret+Proto-Oncogene+Proteins at the US National Library of Medicine Medical Subject Headings (MeSH) ...
Certaines des différentes catégories des oncogenes comprennent : Facteurs de croissance ou mitogènes - ces oncogenes stimulent ... Un exemple dun oncogene dans ce type est c-SiS.. *Récepteurs tyrosine kinase - les exemples des oncogenes dans ce type ... Plusieurs autres systèmes ont été conçus pour classifier des oncogenes. Certaines des différentes catégories des oncogenes ... Ces oncogenes peuvent stimuler la cellule sécréter des facteurs de croissance quand il ne ferait pas normalement ainsi, ...
Oncogenes first identified as genes activated by integration of mouse mammary tumour virus and causing the development of ... Oncogenes first identified as genes activated by integration of mouse mammary tumour virus and causing the development of ...
Oncogene An oncogene is a special type of gene that is capable of transforming host cells and triggering carcinogenesis. The ... Classes of proto-oncogene. There are five major classes of proto-oncogene/oncogenes: (1) growth factors, (2) growth factor ... Inherited oncogenes. In most cases, oncogenes result from changes in proto-oncogenes in select somatic cells and are not passed ... We inherit two of each type of proto-oncogene. A change in only one proto-oncogene of a pair converts it into an oncogene. The ...
Bishop JM (1983) Cellular oncogenes and retroviruses. Ann Rev Biochem 52:301-354PubMedCrossRefGoogle Scholar ... Watt R, Stanton LW, Marcu KB, Gallo RC, Croces CM, Ravena G (1983) Nucleotide sequence of cloned cDNA of human c-myc oncogene. ... Roussel M, Saule S, Lagrou C, Rommens C, Beug H, Graf T, Stehelin D (1979) Three new types of viral oncogene of cellular origin ... Rous Sarcoma Virus Avian Myeloblastosis Virus Cellular Oncogene Avian Sarcoma Virus Murine Sarcoma Virus These keywords were ...
... oncogene: , MYC and RAS). The origin or location of the gene is indicated by the prefix of ... In cancer: Proto-oncogenes and the cell cycle. …can be seen in the ras family of oncogenes. The ras oncogene has a single ... In oncogene. , MYC and RAS). The origin or location of the gene is indicated by the prefix of "v-" for virus or "c-" for cell ... More than 70 human oncogenes have been identified. Breast cancer has been linked to… ...
"But it s the first really definitive link where we can show with biological experiments that microRNAs can act as an oncogene ... Finally, the researchers tested the effects of overexpression of the miRNA cluster in mice carrying the oncogene c-myc -- ... just as cancer-causing genes are called oncogenes. Senior author Scott Hammond of the University of North Carolina at Chapel ...
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. The theory of oncogenes was foreshadowed by the German biologist ... The resultant protein encoded by an oncogene is termed oncoprotein. Oncogenes play an important role in the regulation or ...
RAS oncogenes: weaving a tumorigenic web.. Pylayeva-Gupta Y1, Grabocka E, Bar-Sagi D. ... In this Review, we describe how RAS oncogenes exploit their extensive signalling reach to affect multiple cellular processes ... Hyperproliferative cues from activation of the RAS oncogene can result in replicative stress leading to DNA damage. In response ...
... creating the dominant oncogene BCR/abl at the junction point. The specific function of the BCR/abl fusion protein is not ... 9, creating the dominant oncogene BCR/abl at the junction point. The specific function of the BCR/abl fusion protein is not ...
Thus, the authors conclude that IKBKE is a breast cancer oncogene that may link PI3K signaling to activation of the NF-κB ... Boehm et al. used an integrative genomic approach to identify potential oncogenes by determining which signaling pathways ... IKBKE is a breast cancer oncogene that may link PI3K signaling to activation of the NF-κB pathway. ... IKBKE is a breast cancer oncogene that may link PI3K signaling to activation of the NF-κB pathway. ...
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 ...
From Metabolism to Oncogenes and Back - Part II. Last time I told you about how the view of cancer switched from the ... From Metabolism to Oncogenes and Back - Part I. One of the biggest stories over the last decade was how metabolism taught ... Its components include some of the most important proto-oncogenes and tumor suppressors. One of the major outputs of this ... The first group of genes are called proton-oncogenes, the second group are named tumor suppressor genes. Next we discovered ...
Oncogenes are responsible for encoding proteins that have the ability to kick-start cellular transformation either by ... Oncogenes were initially discovered as cancer-causing viruses. However, science soon proved that they are found in all normal ... The Importance of C-Sis Oncogene. Studies have demonstrated that human c-sis proto-oncogene is over expressed in a large number ... For instance, the c-sis oncogene (or proto-oncogene to be more precise) is actively transcribed in the highly invasive and ...
Oncogene. 1997. [4] Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human ... The BCR-ABL oncogene is a fusion gene resulting from a reciprocal translocation between chromosome 9 and chromosome 22 ( ... is a growth factor receptor encoded by the MPL proto-oncogene. The most frequent MPL mutation in the MPN context is a G to T ... carry a myeloproliferative leukemia virus oncogene (MPL) mutation. The mechanisms, by which these alter cell function and ...
From the pioneering discovery of the first oncogene in a chicken virus, oncogene research has developed into a central topic in ... Oncogenes and proto-oncogenes will remain in the focus of biology, biochemistry, and medicine. ... Principally, any activating mutation or deregulation of cellular oncogenes, also termed proto-oncogenes in their normal ... These novel oncogenes were later shown to be derived from cellular oncogenes, which today are known as major drivers of human ...
Oncogene activation can be detected by immunoblotting for oncogene proteins in serum. This technique has been applied to screen ... Three of the 18 individuals screened were found to have abnormal expression of the proteins of the ras and fes oncogenes. These ... These results suggest the feasibility of using serum oncogene proteins along with DNA-carcinogen adducts as potential molecular ...
Ayalew Tefferi, Juergen Thiele, Attilio Orazi, Hans Michael Kvasnicka, Tiziano Barbui, Curtis A. Hanson, Giovanni Barosi, Srdan Verstovsek, Gunnar Birgegard, Ruben Mesa, John T. Reilly, Heinz Gisslinger, Alessandro M. Vannucchi, Francisco Cervantes, Guido Finazzi, Ronald Hoffman, D. Gary Gilliland, Clara D. Bloomfield and James W. Vardiman ...
... Anticancer Drugs. 2000 Apr;11(4):225-36. doi: 10.1097/00001813-200004000-00001. ... Several lines of evidence suggest that expression of ras oncogenes can confer resistance to cisplatin by reducing drug uptake ... Furthermore, the identification of oncogenes involved in cisplatin resistance has already led to in vitro approaches which ... More recently, additional pathways have been characterized indicating that altered expression of oncogenes that subsequently ...
... triggers the expression of proto-oncogenes, which in turn direct the characteristic increase in protein synthesis. New results ...
Understanding the genetic origin of cancer at the molecular level has facilitated the development of novel targeted therapies. Aberrant activation of the ErbB family of receptors is implicated in many human cancers and is already the target of several anticancer therapeutics. The use of mAbs specific for the extracellular domain of ErbB receptors was the first implementation of rational targeted therapy. The cytoplasmic tyrosine kinase domain is also a preferred target for small compounds that inhibit the kinase activity of these receptors. However, current therapy has not yet been optimized, allowing for opportunities for optimization of the next generation of targeted therapy, particularly with regards to inhibiting heteromeric ErbB family receptor complexes.. ...
... Agarwal, Divyansh Univ Penn, Dept Genom & Computat Biol, Perelman Sch ... Here, we propose that germline polymorphisms can function as oncogenic modifiers, or co-oncogenes, and these determine what ...
Finally, oncogene addiction does not reconcile why oncogene activation in normal cells and oncogene inactivation in tumor cells ... although oncogene addiction does account for why oncogene activation induces apoptosis, it does not account for why oncogene ... Mechanisms of Oncogene Addiction. We proposed that the phenomenon of oncogene addiction is a consequence of the fact that the ... The consequences of oncogene inactivation in a tumor are a direct consequence of the regained ability of that oncogene to now ...
Oncogenes and Tumor Suppressor Genes RT2 Profiler PCR Array The Rat Oncogenes & Tumor Suppressor Genes RT² Profiler PCR Array ... Oncogenes and Tumor Suppressor Genes RT2 Profiler PCR Array The Human Oncogenes & Tumor Suppressor Genes RT² Profiler PCR Array ... Oncogenes and Tumor Suppressor Genes RT2 Profiler PCR Array The Mouse Oncogenes & Tumor Suppressor Genes RT² Profiler PCR Array ... Oncogene Panel 384HT qBiomarker Somatic Mutation PCR Array The Human Oncogene Panel qBiomarker Somatic Mutation PCR Array is a ...
Proto-oncogeneEdit. A proto-oncogene is a normal gene that could become an oncogene due to mutations or increased expression. ... The first confirmed oncogene was discovered in 1970 and was termed sarcom. Sarcoma was in fact first discovered as an oncogene ... Proto-oncogenes code for proteins that help to regulate the cell growth and differentiation. Proto-oncogenes are often involved ... Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead.[3] Most oncogenes began ...
Proto-Oncogenes in Cell Development. Gregory R. Bock (Editor), Joan Marsh (Editor) ... and chemical implications and the latest thinking on the role of proto-oncogenes and their relationship to cell development and ... deterioration in amphibians, the role of the eukaryotic cell cycle, and the role of proto-oncogenes in differentiation and ...
  • An oncogene is a special type of gene that is capable of transforming host cells and triggering carcinogenesis. (
  • oncogene A dominant mutant allele of a cellular gene (a proto-oncogene ) that disrupts cell growth and division and is capable of transforming a normal cell into a cancerous cell. (
  • The BCR-ABL oncogene is a fusion gene resulting from a reciprocal translocation between chromosome 9 and chromosome 22 (Philadelphia chromosome) first described in 1960 [14, 15]. (
  • Similarly, the recognition through cytogenetics of gene amplification units in aggressive forms of certain tumors has helped to define another important type of somatic genetic change in neoplasia, again involving both known and previously unknown oncogenes. (
  • An oncogene is a gene that has the potential to cause cancer. (
  • 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. (
  • A proto-oncogene is a normal gene that could become an oncogene due to mutations or increased expression. (
  • 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. (
  • QIAGEN provides a broad range of assay technologies for oncogene and tumor suppressor gene research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. (
  • The scientists mixed dying rat cells carrying cancer-causing oncogenes with mouse cells lacking p53, a tumor-suppressing gene. (
  • In contrast, however, the rat cells did not transform mouse cells carrying a healthy p53 gene, suggesting that the gene protected the cells from any acquired oncogenes. (
  • However, when mouse cells lacking the p53 gene and carrying the oncogenes were implanted into live mice, the cells became tumorigenic and thrived. (
  • Somatic mutations in a subset of growth hormone (GH)-secreting pituitary tumors convert the gene for the alpha polypeptide chain (alpha s) of Gs into a putative oncogene, termed gsp. (
  • The mutant alpha i2 gene is a putative oncogene, referred to as gip2. (
  • Altered function, in turn, leads to deregulated mitogenic survival and growth of tumors that frequently exhibit oncogene-activating genomic alterations such as gene amplification or gain-of-function point mutations. (
  • Specifically, the identified molecule is produced in a cancer-causing gene (SMYD3) as its role in healthy cells is to inhibit pro-cancer action of the oncogene. (
  • DLX5, a gene crucial for embryonic development, promotes cancer by activating the expression of the known oncogene, MYC, according to researchers from Fox Chase Cancer Center. (
  • Previously the researchers found that a chromosomal inversion "" a genetic misalignment, where part of the chromosome containing the DLX5 gene gets flipped around during cell division "" cooperates with another known oncogene, AKT2, to drive cancer in mice. (
  • Viral Oncogenes that are homologues of erbA1 (THRA) Gene which encodes Thyroid Hormone Receptor alpha. (
  • Eventually this normal gene mutated into an abnormally functioning oncogene within the Rous sarcoma virus. (
  • An oncogene is a modified gene , or a set of nucleotides that codes for a protein and is believed to cause cancer . (
  • Human oncogenes should be expressed according to style for human gene symbols (see , Human Gene Nomenclature). (
  • Their articles thoroughly explicate the premises, principles, techniques, and approaches to oncogene targeting in various types of human cancer by using signal transduction inhibitors, immunological targeting methods, and antisense gene therapy. (
  • Oncogenes are responsible for encoding proteins that have the ability to kick-start cellular transformation either by activating mutations or by over expression. (
  • This strong selective pressure for the emergence of cells that carry de novo mutations in the respective oncogenes indicates the remarkable dependence of these neoplastic cells on specific oncogenes, because in principle, the cells could have become resistant by de novo mutations in other oncogenes. (
  • As a genetic disease, cancer is primarily caused by mutations in oncogenes and tumor suppressors, which serve to control tissue homeostasis [ 1 ]. (
  • Genetic mutations resulting in the activation of oncogenes increase the chance that a normal cell will develop into a tumor cell. (
  • Mutations in microRNAs can lead to activation of oncogenes. (
  • An axiom in cancer research is that the multistage process of tumor formation ( 1 ) is driven by progressive acquisition of activating mutations in dominant growth-enhancing genes (oncogenes [ HN2 ]) and inactivating mutations in recessive growth-inhibitory genes (tumor suppressor genes [ HN3 ]) ( 2 ). (
  • Oncogenes can work in concert to produce cancer, and their action may be exacerbated by retroviruses, jumping genes, or inherited genetic mutations. (
  • SAN DIEGO--( BUSINESS WIRE )--Turning Point Therapeutics, Inc., a clinical-stage precision oncology company designing and developing novel drugs to address treatment resistance, presented data from four studies at AACR 2019, highlighting potent activity of its kinase inhibitors, including repotrectinib against targeted oncogene drivers and many of their resistance mutations, and TPX-0022, a novel MET/CSF1R/SRC inhibitor. (
  • The ras oncogene has a single defect in its nucleotide sequence, and, as a result, there is a change of a single amino acid in the protein for which it encodes. (
  • Myeloproliferative leukaemia protein (MPL), also termed thrombopoietin receptor, is a growth factor receptor encoded by the MPL proto-oncogene. (
  • Here we examine the hypothesis that an increase in cytosolic free Ca2+ concentration ([Ca2+]i) triggers the expression of proto-oncogenes, which in turn direct the characteristic increase in protein synthesis. (
  • The resultant protein encoded by an oncogene is termed oncoprotein. (
  • Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. (
  • Blood samples were obtained from all workers and analyzed for PAH-DNA adducts and protein products encoded by nine specific oncogenes. (
  • Overall, four samples were demonstrated to be positive for a specific oncogene protein product. (
  • The cases in which oncogene encoded protein products were identified came from one individual with high exposure and another with a medium level of exposure. (
  • The authors speculate that the two workers who tested positive for oncogene protein products and had high levels of PAH-DNA adducts have a high probability of developing malignant disease. (
  • Newswise - Cancer researchers have discovered surprising new functions for a protein called MYC, a powerful oncogene that is estimated to drive the development of almost half a million new cancer cases in the US every year. (
  • The identified anti-oncogene is along non-coding ribonucleic acid (lncRNA), ie a molecule that does not produce protein itself but is responsible for regulating the expression of other proteins. (
  • After it was established that cancer-causing retroviruses carry oncogenes, the first important step was to define the protein product coded by each of them. (
  • The protein product of this oncogene, which has a unique pattern of enzyme, drastically alters the biochemistry of the cell and diminishes its capacity for responding to regulatory signals from hormones. (
  • To Dr. Erikson, first to discover the protein product of an oncogene and to provide a model for other investigators to employ in their search for the products of other oncogenes-a pioneer within a field of pioneers-this 1982 Albert Lasker Basic Medical Research Award is given. (
  • Our group has a long-standing interest in the c-myc oncogene and its product, the Myc protein. (
  • It interacts with a wide variety of proteins, such as apoptosis antigen Fas, centromere protein C, and transcription factor erythroblastosis virus E26 oncogene homolog 1 (ETS1). (
  • So, in humans, there are two unique ways in which oncogenesis occurs, by true viral infection and by mutation of proto-oncogenes that already exist in human cells. (
  • These sequences, termed viral oncogenes ( v-onc ), originated from the normal cellular genome (B ishop and V armus 1982). (
  • The efficacy of this strategy requires novel methods, including integrative genomics and systems biology, to identify the state of oncogene addiction (i.e., the "Achilles heel") in specific cancers. (
  • Combination therapy may also be required to prevent the escape of cancers from a given state of oncogene addiction. (
  • We introduced the concept of "oncogene addiction" to emphasize this apparent dependency of some cancers on one or a few genes for the maintenance of the malignant phenotype ( 1 , 2 , 5 , 6 ). (
  • The most convincing evidence for the concept of oncogene addiction comes from the increasing number of examples of the therapeutic efficacy of antibodies or drugs that target specific oncogenes in human cancers ( Table 1 ). (
  • Oncogene addiction is a process in which cancers with genetic, epigenetic, or chromosomal irregularities become dependent on one or several genes for maintenance and survival. (
  • They have identified what apparently is an oncogene associated with some colorectal cancers. (
  • But, based on their findings, published online in PLoS ONE , the scientists suggest E-cadherin can also function as an oncogene in some cancers. (
  • Alexander Drilon, M.D., Clinical Director of the Early Drug Development Service at Memorial Sloan Kettering Cancer Center and an investigator in the Phase 1 portion of the ongoing TRIDENT-1 study of repotrectinib, said, "As physicians adopt next-generation sequencing to identify genomic alterations in different cancers, there is an increased need for precision therapies that target specific oncogenes, such as TRK and ROS1. (
  • It's components include some of the most important proto-oncogenes and tumor suppressors. (
  • Whether due to changes in regulatory tumor suppressors/oncogenes or by acting as metabolic oncogenes themselves, enzymes involved in the complex network of metabolic pathways are being studied to understand their role and assess their utility as therapeutic targets. (
  • Over the past 10-20 years, increasing evidence has shown that the majority of oncogenes and tumor suppressors also play a role in the regulation of metabolism. (
  • There is much evidence to support the notion that loss of tumor suppressors or gain of oncogenes can lead to cancer. (
  • A good example of an oncogene is CDK8: Cyclin-dependent kinase 8. (
  • Numerous studies using human cancer cell lines indicate that although these cells are aneuploid and carry several genetic and epigenetic abnormalities, they can also be highly dependent on the activity of a single oncogene for continued cell proliferation and survival ( Table 1 ). (
  • Genetic differences in oncogenes and/or TSGs in tumor samples may correlate with biological phenotypes or clinical outcomes such as staging, therapy selection, metastasis, or survival rate. (
  • A new candidate oncogene for ovarian cancer emerges from a genome-wide scan of both common and rare genetic variants. (
  • This is the concept of oncogene addiction, the elucidation of which has led to substantial progress in therapeutic interventions. (
  • In addition, the uncontrolled proliferation of stromal fibroblasts in breast tumors with desmoplasia are considered a direct consequence of the over expression of c-sis and similar oncogenes. (
  • With research establishing the fact that human c-sis oncogene is expressed in many types of tumors and carcinomas, efforts have been made to develop appropriate therapy that can stop the overexpression of the c-sis oncogene in pathological conditions. (
  • 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. (
  • Examples include imatinib, which targets the bcr-abl oncogene in chronic myeloid leukemia and also targets the c-kit oncogene in gastrointestinal stromal tumors, and gefitinib and erlotinib, which target the epidermal growth factor receptor (EGFR) in non-small cell lung carcinoma (NSCLC), pancreatic cancer, and glioblastoma. (
  • A common point in all human tumors is that they produce an activation of oncogenes, genes that cause cancer and they also cause a loss of function of the protective genes, called anti-oncogenes or tumor suppressor genes. (
  • Example of three colon tumors (up) whose growth was inhibited (down) a molecule of RNA (ribonucleic acid) which acts as identified anti-oncogene. (
  • We believe this discovery will be the starting point to find many other oncogenes and anti-oncogenes that coexist in regions of our genome, that when their life together deteriorates, contribute to the development of human tumors," said Dr. Esteller. (
  • To Dr. Hanafusa, whose studies combining scientific imagination with meticulous laboratory techniques showed the mechanism by which retroviruses take oncogenes from normal cells and thus acquire the ability to cause malignant tumors, this 1982 Albert Lasker Basic Medical Research Award is given. (
  • JACKSONVILLE, Fla. - Researchers at Mayo Clinic in Florida have found that a molecule long believed to be a beneficial tumor suppressor - and thus a potential cancer drug target - appears to act as an oncogene in some lethal brain tumors . (
  • E-cadherin expressed in glioblastoma functioned like an oncogene and it could be doing the same in many breast, ovarian, and other tumors found elsewhere in the body. (
  • Although this is a relatively common mechanism of oncogenesis in animals, very few oncogene-carrying viruses have been identified in man. (
  • Oncogenes and tumor suppressor genes (TSGs) both play a role in oncogenesis via opposite mechanisms. (
  • The Human Oncogenes & Tumor Suppressor Genes RT² Profiler PCR Array profiles the expression of 84 key genes that promote oncogenesis. (
  • The Mouse Oncogenes & Tumor Suppressor Genes RT² Profiler PCR Array profiles the expression of 84 key genes that promote oncogenesis. (
  • The Rat Oncogenes & Tumor Suppressor Genes RT² Profiler PCR Array profiles the expression of 84 key genes that promote oncogenesis. (
  • The Oncogenes and Tumor Suppressor Antibody Sampler Kit offers an economical means of investigating proteins commonly involved in the biological pathways behind oncogenesis, tumor metastasis, and cancer pathology. (
  • Oncogenesis is a multistep process leading to sequential alterations in several oncogenes, tumor-suppressor genes, and microRNA genes (1,2). (
  • In Oncogene-Directed Therapies, prominent investigators and clinicians, several of them pioneers in the field, summarize what is known about oncogenes and oncogenesis-in a balanced blend of fundamental science, basic research, experimental therapeutics, and early clinical experience-and describe how that knowledge can be used to treat the disease. (
  • used an integrative genomic approach to identify potential oncogenes by determining which signaling pathways downstream of oncogenic Ras contribute to cell transformation. (
  • More recently, additional pathways have been characterized indicating that altered expression of oncogenes that subsequently limit the formation of cisplatin-DNA adducts and activate anti-apoptotic pathways may also contribute to the resistance phenotype. (
  • However, because resistance mechanisms often emerge, explicating the pathways that connect therapeutic oncogene inactivation to the cell death machinery is critical to exploiting additional synthetic lethal opportunities. (
  • Hannon and Lowe, who were recently appointed as HHMI investigators at Cold Spring Harbor Laboratory, say that given the new findings, they agree with a proposal calling for cancer-causing microRNAs to be dubbed "oncogenic micro RNAs," or "oncomiRs," just as cancer-causing genes are called oncogenes. (
  • These genes are called proto-oncogenes. (
  • Such genes are called oncogenes. (
  • Dr. Erikson isolated the first one-the enzyme coded by the avian sarcoma virus oncogene. (
  • These results suggest the feasibility of using serum oncogene proteins along with DNA-carcinogen adducts as potential molecular epidemiological markers in exposed worker populations. (
  • An inquiry into the carcinogenic predictive value of serum oncogene proteins was conducted for an occupational cohort with known exposure to benzo(a)pyrene (50328) and other polycyclic aromatic hydrocarbons (PAHs). (
  • It turns out that by regulating how the ribosome translates different mRNAs, TOR signalling can upregulate the expression of a whole slew of proto-oncogenes. (
  • There is also normal expression of c-sis oncogene in human and bovine endothelial cells. (
  • There is also an enhanced expression of c-sis oncogenes in human meningiomas and neurinomas. (
  • Steroid modulation of the expression of growth factor and oncogenes in breast cancer. (
  • Three of the 18 individuals screened were found to have abnormal expression of the proteins of the ras and fes oncogenes. (
  • Dependence on the continued expression of other oncogenes for the maintenance of the neoplastic state has also been seen in other tissues in murine models ( Table 1 ). (
  • Further study of one insertion, somatically acquired in primary leukaemia tumour genomes, reveals that it nucleates formation of an active enhancer that drives expression of the LMO2 oncogene. (
  • Upon cucurbitacin B treatment, upregulation of DNMT1 and obvious heavy methylation in the promoters of c-Myc, cyclin D1, and survivin, which consequently downregulated the expression of all these oncogenes, were observed. (
  • Berberine suppressed the RET proto-oncogene expression by more than 90 % in medullary thyroid carcinomas cells. (
  • This phenomenon, called "oncogene addiction," provides a rationale for molecular targeted therapy. (
  • aims to bring together leading academic scientists, researchers and research scholars to exchange and share their experiences and research results on all aspects of Molecular Biology of Oncogenes. (
  • Also, high quality research contributions describing original and unpublished results of conceptual, constructive, empirical, experimental, or theoretical work in all areas of Molecular Biology of Oncogenes are cordially invited for presentation at the conference. (
  • ICMBO 2020 has teamed up with the Special Journal Issue on Molecular Biology of Oncogenes . (
  • ZNF703 is a common Luminal B breast cancer oncogene that differentially regulates luminal and basal progenerators in human mammary epithelium , (2011) EMBO Molecular Medicine , DOI: 10.1002/emmm.201100122. (
  • Oncogene-induced replication stress and its role in cancer development have been studied comprehensively, however its molecular basis is still unclear. (
  • Rather, these new agents have emerged directly from molecular analysis of various cancer-causing genes (oncogenes). (
  • Unique in perspective and comprehensive in its coverage, Oncogene-Directed Therapies not only integrates for all those engaged in-or simply interested in the cutting-edge of-"the war on cancer" the many remarkable recent achievements in our molecular understanding and treatment of these diseases, but also clarifies what directions future research might optimally take, as well as what significant accomplishments might lie ahead. (
  • Oncogenes and Growth Factors Abstracts covers every aspect of oncogene research into the molecular basis of malignant transformations. (
  • Oncogenes were first discovered in retroviruses ( viruses containing the enzyme reverse transcriptase, and RNA , rather than DNA ) that were found to cause cancer in many animals (e.g., feline leukemia virus, simian sarcoma virus). (
  • The first confirmed oncogene was discovered in 1970 and was termed SRC (pronounced "sarc" as it is short for sarcoma). (
  • Sarcoma was in fact first discovered as an oncogene in a chicken retrovirus . (
  • Experiments performed by Dr. G. Steve Martin of the University of California, Berkeley demonstrated that the sarcoma was indeed the oncogene of the virus. (
  • Jain and colleagues ( 5 ) engineered a conditional transgenic mouse to overexpress the myc oncogene [ HN8 ], which induced formation of highly malignant osteogenic sarcoma. (
  • With research proving the role of c-sis oncogene in vascularization processes, some researchers also suggest that c-sis oncogene plays a role in the pathogenesis of atherosclerosis. (
  • Researchers are attempting to isolate anti-oncogenes that suppress tumours and may be used in the treatment of cancer. (
  • Using clues from prior studies, the researchers reasoned that regulatory features and genome organization changes may contribute to the cancer-promoting impact of oncogene-containing DNA amplifications. (
  • By isolating certain genes in a cancer cell, called oncogenes, researchers hope to be able to affect the lifespan and proliferation of certain cancer cells. (
  • Oncogenes and Growth Factors Abstracts will also be valuable to researchers in immunology, virology, bacteriology, genetics, and other related fields. (
  • Here, we review the current understanding of replication regulation, its potential disruption and how oncogenes perturb the replication and induce DNA damage leading to genomic instability in cancer. (
  • Anti-oncogenes are genes that may turn off cancer cells, and transform them back to normal cells. (
  • Usually multiple oncogenes, along with mutated apoptotic or tumor suppressor genes will all act in concert to cause cancer. (
  • Cancer cells acquire abnormalities in multiple oncogenes and tumor suppressor genes (A, B, C, and D). Inactivation of a single critical oncogene (A) can induce cancer cells to differentiate into cells with a normal phenotype or to undergo apoptosis. (
  • Cellular homologs (c -one ) of 20 different retroviral oncogenes have now been identified in a variety of species throughout the vertebrate phylum (Table 1) (S tehelin et al. (
  • Bishop and Varmus were awarded the Nobel Prize in Physiology or Medicine in 1989 for their discovery of the cellular origin of retroviral oncogenes. (
  • Proto-oncogenes code for proteins that help to regulate the cell growth and differentiation. (
  • The collected data explores the biological, medical, and chemical implications and the latest thinking on the role of proto-oncogenes and their relationship to cell development and deterioration in amphibians, the role of the eukaryotic cell cycle, and the role of proto-oncogenes in differentiation and development. (
  • This interaction varies among proliferation and differentiation states and can be affected by multiple factors, including oncogenes. (
  • v-erbA Oncogenes potentiate the transforming ability of other Oncogenes such as v-erbB by inhibiting spontaneous differentiation of already transformed Cells . (
  • Oncogenes and tumor suppressor genes are important not only for cell proliferation but also for cell fate determination [ HN5 ] (differentiation, senescence, and apoptosis), their effects often depending on the type of cell in which they are expressed. (
  • The RET proto-oncogene encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor (GDNF) family of extracellular signalling molecules . (
  • Forgotten since classic animal studies in the 1980s, the role of PHGDH as a potential therapeutic target and putative metabolic oncogene has recently reemerged following publication of two prominent papers near-simultaneously in 2011. (
  • However, MYC is an especially complex oncogene that has resisted therapeutic manipulation to date. (
  • Prive GG, Melnick A. Specific peptides for the therapeutic targeting of oncogenes. (
  • Cancer revoked: oncogenes as therapeutic targets. (
  • Oncogenes and Growth Factory Abstracts enables scientists to keep abreast of both experimental and clinical literature focusing on mechanisms of oncogenes and growth factors. (
  • Alitalo K, Schwab M, Lin CL, Varmus HE, Bishop JM (1983) Homogenously staining chromosomal regions contain amplified copies of an abundantly expressed cellular oncogene (c -myc ) in malignant neuroendocrine cells from a human colon carcinoma. (
  • Translocation, point mutation, and amplification are some means by which proto-oncogenes are converted to malignant oncogenes. (
  • Other non-malignant diseases linked to this oncogene are giant cell arteritis, bronchiolitis obliterans, as well as different fibrotic events. (
  • Here, we propose that germline polymorphisms can function as oncogenic modifiers, or co-oncogenes, and these determine what complementary subsequent somatic events are required for full malignant transformation. (
  • The theory of oncogenes was foreshadowed by the German biologist Theodor Boveri in his 1914 book Zur Frage der Entstehung Maligner Tumoren ('The Origin of Malignant Tumours'), Gustav Fisher, Jena, 1914. (
  • A tantalizing question still under debate is whether an oncogene that is crucial for the initial development of a specific tumor is required for maintaining the malignant phenotype of that tumor. (
  • These findings are consistent with other data showing that cancer cells are often "addicted to" (that is, physiologically dependent on) the continued activity of specific activated or overexpressed oncogenes for maintenance of their malignant phenotype. (
  • For example, Felsher and Bishop ( 6 ) showed that transgenic mice expressing the myc oncogene in hematopoietic cells developed malignant T cell leukemias and acute myeloid leukemias. (
  • Conversion of a protooncogene to an oncogene by amplification, translocation, or point mutation can lead to unrestrained cellular proliferation and malignant change. (
  • As a direct consequence of such changes, activated oncogenes may lead to abnormal cell proliferation and hence tumor development. (
  • Once such therapy for abnormal proliferation of the c-sis oncogene is the triplex forming oligonucleotides (TFO). (
  • Most oncogenes began as proto-oncogenes: normal genes involved in cell growth and proliferation or inhibition of apoptosis. (
  • NEW YORK - Non-coding regulatory sequences can get co-amplified with extrachromosomal oncogenes in cancer, new research suggests, producing circularized structures with altered connections that may be selected to boost the proliferation of these tumor cells. (
  • Oncogenes are genes in a cancer cell that influence the mutation, amplification, and proliferation of the cell. (
  • If a cell that usually does not produce growth factors suddenly starts to do so (because it developed an oncogene), it will thereby induce its own uncontrolled proliferation ( autocrine loop ), as well as the proliferation of neighboring cells. (
  • In the same year, a marvelous synergistic effort of biochemistry and virus genetics led to the first physical identification of an oncogene, reported in the classic paper by Duesberg and Vogt in PNAS ( 1 ). (
  • Collectively, our results uncover an additional layer of regulatory complexity in canonical driver events, which may provide avenues for the targeted disruption of key oncogenes that have been considered undruggable to date," senior and co-corresponding author Peter Scacheri, a researcher in the department of genetics and genome sciences at Case Western Reserve University School of Medicine, and his co-authors wrote. (
  • A study coordinated by Manel Esteller, Director of the program of epigenetics and cancer biology at the Bellvitge Institute for Biomedical Research (IDIBELL), Professor of genetics at the University of Barcelona and ICREA researcher, has discovered the existence of an antitumor molecule that originates within an oncogene. (
  • Studies of humans led to the discovery of related genes called proto-oncogenes that exist naturally in the human genome. (
  • More than 70 human oncogenes have been identified. (
  • For instance, the c-sis oncogene (or proto-oncogene to be more precise) is actively transcribed in the highly invasive and proliferative cytotrophoblastic shell during the first trimester of pregnancy in the human placenta. (
  • Studies have demonstrated that human c-sis proto-oncogene is over expressed in a large number of human tumor cells, establishing an autocrine growth-promoting circuit. (
  • These studies have also provided evidence for many previously unidentified human oncogenes. (
  • Since the 1970s, dozens of oncogenes have been identified in human cancer. (
  • Dr. Robert Weinberg is credited with discovering the first identified human oncogene in a human bladder cancer cell line. (
  • The Human Oncogene Panel qBiomarker Somatic Mutation PCR Array is a translational research tool that allows rapid, comprehensive, and accurate profiling of the somatic mutation status of 36 key. (
  • The Bayreuth biochemist Dr. Claus-D. Kuhn and his research team have deciphered how the important human oncogene CDK8 is activated in cells of healthy individuals. (
  • Your search returned 1 Cbl proto-oncogene C ELISA ELISA Kit across 1 supplier. (
  • Your search returned 468 KRAS proto-oncogene, GTPase Antibodies across 39 suppliers. (
  • Certain oncogenes of vertebrates are derived from viruses (see oncogenic ). (
  • Thus, in a transgenic mouse model, switching on the c-myc oncogene in the hematopoietic cells led to the development of T-cell and myeloid leukemias. (
  • Oncogenes were initially discovered as cancer-causing viruses. (
  • Oncogenes were discovered and characterized in viruses and animal experimental systems. (
  • Despite this complexity, their growth and survival can often be impaired by the inactivation of a single oncogene. (
  • Examples of inhibitors that have been used to block oncogenes and disrupt oncogene addiction include imatinib, nilotinib, dasatinib, and ponatinib, among others. (
  • As they reported online today in Cell , Scacheri and his colleagues started with a computational strategy to find co-amplification of oncogene-regulatory sequence in glioblastoma (GBM), using targeted sequencing, CRISPR-based screening, and other methods to take a closer look at EGFR-containing amplifications. (
  • Proto-oncogenes typically encode proteins involved in positive control of the cell division cycle, such as growth factor receptors, signal transduction proteins, and transcription factors. (
  • The original and unmutated (wild-type) allele of a certain oncogene is referred to as the proto-oncogene, which has the propensity to promote cell growth and cell division. (
  • The activation of the c-sis proto-oncogene (which has a striking homology to platelet-derived growth factor [PDGF]) is linked to the autocrine stimulation of cell growth in the breasts. (
  • Cell calcium, oncogenes, and hypertrophy. (
  • Oncogenes play an important role in the regulation or synthesis of proteins linked to tumorigenic cell growth. (
  • Proto-oncogenes promote normal cell growth. (
  • Oncogenes from a dying cell can be transferred to a nearby cell via phagocytosis, a process through which one cell engulfs another. (
  • If the recipient cell is already genetically unstable, the newly acquired oncogenes can lead to tumor formation. (
  • The oncogenes were only passed from one generation to the next if they were beneficial to the life of the cell. (
  • If normal genes promoting cellular growth, through mutation, are up-regulated, (gain of function mutation) they will predispose the cell to cancer and are thus termed oncogenes. (
  • Among the 102 tumour cell genomes we analyse, small insertions are frequently observed in enhancer DNA sequences near known oncogenes. (
  • Scientists from the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) and Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM) have now shown that this process is regulated by the MYC oncogene. (
  • In this study, we explore the influence of cucurbitacin B fromon the methylation status at the promoter of oncogenes c-Myc, cyclin D1, and survivin in breast cancer cell lines. (
  • This proto-oncogene may play a role in the regulation of embryonic development and cell growth. (
  • Cancer cell dependence on activated oncogenes is therapeutically targeted, but acquired resistance is virtually unavoidable. (
  • This is the first time in over five years that scientists have discovered a new breast cancer ' oncogene ' - cancer-causing genes that when overactive upset the normal checks and balances that control when and how often a cell divides. (
  • Thus, overexpression of a given oncogene can enhance growth in one cell type but inhibit growth or induce apoptosis [ HN6 ] in another ( 2 - 4 ). (
  • Our study provides the rationale for targeting the NRP1-dependent upregulation of tyrosine kinases, which are responsible for loss of responsiveness to oncogene-targeted therapies. (
  • Examples of proto-oncogenes include growth factors, tyrosine kinases, regulatory GTPases, and transcription factors. (
  • Furthermore, the identification of oncogenes involved in cisplatin resistance has already led to in vitro approaches which successfully inactivated these genes using ribozymes or antisense oligodeoxynucleotides, thus restoring cisplatin sensitivity. (
  • Holmgren and colleagues also report that in vitro , the acquired oncogenes were lost from the cells after a few generations. (
  • In vitro , the oncogenes conferred no advantage and were discarded. (
  • There are, however, several examples of a true escape from a given state of oncogene addiction. (
  • A prime example of a cancer that exhibits oncogene addiction is chronic myelogenous leukemia (CML), which is driven by a mutant oncogene known as the Philadelphia chromosome. (
  • Oncogene addiction can be treated by using enzyme inhibitor therapy. (
  • It could be argued that all of these results are peculiar to transgenic mice with leukemia or cancer, because in these models the engineered oncogene plays an unusually potent role in the neoplastic process. (
  • Colon Cancer Oncogene Discovered ( CDK8 is frequently amplified in these. (
  • Dr. Bishop extended his studies by showing that this was only the first of a number of distinct oncogenes expressed at inappropriate levels in neoplastic tissues. (
  • Thus, the authors conclude that IKBKE is a breast cancer oncogene that may link PI3K signaling to activation of the NF-κB pathway. (
  • Such events were not limited to GBM, the team reported, noting that similar oncogene co-amplifications appeared to occur in breast cancer, medulloblastoma, and other cancer types based on additional experiments and analyses. (
  • To induce diapause or to put embryonic stem cells into a dormant state, it is therefore sufficient to deactivate the MYC oncogene, Trumpp summarizes. (