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Oncogene
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==Classification== There are several systems for classifying oncogenes,<ref>{{Cite web |url=http://web.indstate.edu/thcme/mwking/oncogene.html#classes |title=THE Medical Biochemistry Page<!-- Bot generated title --> |access-date=2007-03-12 |archive-date=2021-01-26 |archive-url=https://web.archive.org/web/20210126060626/https://web.indstate.edu/thcme/mwking/oncogene.html#classes |url-status=dead }}</ref> but there is not yet a widely accepted standard. They are sometimes grouped both spatially (moving from outside the cell inwards) and chronologically (parallelling the "normal" process of signal transduction). There are several categories that are commonly used: {| class="wikitable" ! Category !! Examples !! Cancers !! Gene functions |- | [[Growth factor]]s, or mitogens || [[c-Sis]] ||[[glioblastoma]]s, [[fibrosarcoma]]s, [[osteosarcoma]]s, [[breast carcinoma]]s, and [[melanoma]]s<ref name="pmid2655888">{{cite journal | vauthors = Press RD, Misra A, Gillaspy G, Samols D, Goldthwait DA | title = Control of the expression of c-sis mRNA in human glioblastoma cells by phorbol ester and transforming growth factor beta 1 | journal = Cancer Research | volume = 49 | issue = 11 | pages = 2914β2920 | date = June 1989 | pmid = 2655888 }}</ref> || induces cell proliferation. |- | [[Receptor tyrosine kinases]] || [[epidermal growth factor receptor]] (EGFR), [[platelet-derived growth factor receptor]] (PDGFR), and [[vascular endothelial growth factor]] receptor (VEGFR), [[HER2/neu]] ||Breast cancer, gastrointestinal stromal tumours, non-small-cell lung cancer and pancreatic cancer<ref>{{cite journal | vauthors = Gschwind A, Fischer OM, Ullrich A | title = The discovery of receptor tyrosine kinases: targets for cancer therapy | journal = Nature Reviews. Cancer | volume = 4 | issue = 5 | pages = 361β370 | date = May 2004 | pmid = 15122207 | doi = 10.1038/nrc1360 | s2cid = 6939454 }}</ref> || transduce signals for cell growth and differentiation. |- | Cytoplasmic [[tyrosine kinases]] || [[Src (gene)|Src]]-family, [[Syk-ZAP-70]] family, and [[Bruton's tyrosine kinase|BTK]] family of tyrosine kinases, the Abl gene in CML - [[Philadelphia chromosome]] ||colorectal and breast cancers, melanomas, ovarian cancers, gastric cancers, head and neck cancers, pancreatic cancer, lung cancer, brain cancers, and blood cancers<ref>{{cite journal | vauthors = Summy JM, Gallick GE | title = Src family kinases in tumor progression and metastasis | journal = Cancer and Metastasis Reviews | volume = 22 | issue = 4 | pages = 337β358 | date = December 2003 | pmid = 12884910 | doi = 10.1023/A:1023772912750 | s2cid = 12380282 }}</ref> || mediate the responses to, and the activation receptors of cell proliferation, migration, differentiation, and survival<ref>{{cite journal | vauthors = Thomas SM, Brugge JS | title = Cellular functions regulated by Src family kinases | journal = Annual Review of Cell and Developmental Biology | volume = 13 | issue = 1 | pages = 513β609 | date = 1 November 1997 | pmid = 9442882 | doi = 10.1146/annurev.cellbio.13.1.513 }}</ref> |- | Cytoplasmic [[Serine/threonine kinases]] and their regulatory subunits || [[c-Raf|Raf kinase]], and [[cyclin-dependent kinase]]s (through [[overexpression]]). ||malignant melanoma, papillary thyroid cancer, colorectal cancer, and ovarian cancer<ref>{{cite journal | vauthors = Garnett MJ, Marais R | title = Guilty as charged: B-RAF is a human oncogene | journal = Cancer Cell | volume = 6 | issue = 4 | pages = 313β319 | date = October 2004 | pmid = 15488754 | doi = 10.1016/j.ccr.2004.09.022 | doi-access = free }}</ref>|| involved in organism development, cell cycle regulation, cell proliferation, differentiation, cells survival, and apoptosis<ref>{{cite journal | vauthors = Leicht DT, Balan V, Kaplun A, Singh-Gupta V, Kaplun L, Dobson M, Tzivion G | title = Raf kinases: function, regulation and role in human cancer | journal = Biochimica et Biophysica Acta (BBA) - Molecular Cell Research | volume = 1773 | issue = 8 | pages = 1196β1212 | date = August 2007 | pmid = 17555829 | pmc = 1986673 | doi = 10.1016/j.bbamcr.2007.05.001 }}</ref> |- | Regulatory [[GTPase]]s || [[Ras protein]] ||adenocarcinomas of the pancreas and colon, thyroid tumors, and myeloid leukemia<ref>{{cite journal | vauthors = Bos JL | title = ras oncogenes in human cancer: a review | journal = Cancer Research | volume = 49 | issue = 17 | pages = 4682β4689 | date = September 1989 | pmid = 2547513 }}</ref> || involved in signalling a major pathway leading to cell proliferation.<ref>{{cite journal | vauthors = Hilgenfeld R | title = Regulatory GTPases | journal = Current Opinion in Structural Biology | volume = 5 | issue = 6 | pages = 810β817 | date = December 1995 | pmid = 8749370 | doi = 10.1016/0959-440X(95)80015-8 }}</ref> |- | [[Transcription factor]]s || [[myc]] gene ||malignant T-cell lymphomas and acute myeloid leukemias, breast cancer, pancreatic cancer, retinoblastoma, and small cell lung cancer<ref>{{cite journal | vauthors = Felsher DW, Bishop JM | title = Reversible tumorigenesis by MYC in hematopoietic lineages | journal = Molecular Cell | volume = 4 | issue = 2 | pages = 199β207 | date = August 1999 | pmid = 10488335 | doi = 10.1016/S1097-2765(00)80367-6 | doi-access = free }}</ref> || regulate transcription of genes that induce cell proliferation. |- |[[Coactivator (genetics)|Transcriptional coactivators]] |[[YAP1|YAP]], [[WWTR1]] genes |glioma, melanoma, lung cancer, breast cancers, and more<ref>{{Cite journal |last1=Zanconato |first1=Francesca |last2=Cordenonsi |first2=Michelangelo |last3=Piccolo |first3=Stefano |date=2016-06-13 |title=YAP/TAZ at the Roots of Cancer |journal=Cancer Cell |language=English |volume=29 |issue=6 |pages=783β803 |doi=10.1016/j.ccell.2016.05.005 |issn=1535-6108 |pmc=6186419 |pmid=27300434}}</ref> |interact with transcription factor partners to regulate transcription of genes that induce cell proliferation. |} Additional oncogenetic regulator properties include: ::*Growth factors are usually [[secretion|secreted]] by either specialized or non-specialized cells to induce cell proliferation in themselves, nearby cells, or distant cells. An oncogene may cause a cell to secrete growth factors even though it does not normally do so. It will thereby induce its own uncontrolled proliferation (''[[autocrine loop]]''), and proliferation of neighboring cells, possibly leading to tumor formation. It may also cause production of growth hormones in other parts of the body. ::*[[Receptor tyrosine kinase]]s add phosphate groups to other proteins in order to turn them on or off. Receptor kinases add phosphate groups to receptor proteins at the surface of the cell (which receives protein signals from outside the cell and transmits them to the inside of the cell). Tyrosine kinases add phosphate groups to the amino acid tyrosine in the target protein. They can cause cancer by turning the receptor permanently on (constitutively), even without signals from outside the cell. ::*Ras is a small GTPase that hydrolyses GTP into GDP and phosphate. Ras is activated by growth factor signaling (i.e., EGF, TGFbeta) and acting as a binary switch (on/off) in growth signaling pathways. Downstream effectors of Ras include three mitogen-activated protein kinases Raf a MAP Kinase Kinase Kinase (MAPKKK), MEK a MAP Kinase Kinase (MAPKK), and ERK a MAP Kinase(MAPK), which in turn regulate genes that mediate cell proliferation.<ref>{{cite journal | vauthors = Cargnello M, Roux PP | title = Activation and function of the MAPKs and their substrates, the MAPK-activated protein kinases | journal = Microbiology and Molecular Biology Reviews | volume = 75 | issue = 1 | pages = 50β83 | date = March 2011 | pmid = 21372320 | pmc = 3063353 | doi = 10.1128/MMBR.00031-10 }}</ref>
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