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[[File:Oncogenes illustration.jpg|thumb|300px|Illustration of how a normal cell is converted to a cancer cell, when an oncogene becomes activated]]

An '''oncogene''' is a [[gene]] that has the potential to cause [[cancer]].<ref name=Oncogenes>Wilbur, Beth (ed) 2009. ''The world of the cell''. 7th ed, San Francisco.</ref> Or, equally good, an oncogene is a gene which brings about uncontrolled [[cell division]].<ref>King R.C. Stansfield W.D. & Mulligan P.K. 2006. ''A dictionary of genetics''. 7th ed, Oxford University Press, p309. {{ISBN|0-19-530761-5}}</ref>

Oncogenes in [[tumor]] cells are often [[mutation|mutated]] or [[Gene expression|expressed]] at high levels.<ref name=Kimball>[http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/O/Oncogenes.html Kimball's Biology Pages.] {{Webarchive|url=https://web.archive.org/web/20171231184143/http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/O/Oncogenes.html |date=2017-12-31 }} "Oncogenes" Free full text</ref>

Most normal cells undergo a programmed form of death ([[apoptosis]]). Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead.<ref>[http://nobelprize.org/nobel_prizes/medicine/laureates/2002/illpres/implications.html The Nobel Prize in Physiology or Medicine 2002.] Illustrated presentation.</ref> Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection, to cause [[cancer]]. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the proteins coded by oncogenes.<ref name=Kimball/><ref>{{cite journal |author=Croce C.M |title=Oncogenes and cancer |journal=N Engl J Med. |volume=358 |issue=5 |pages=502–11 |date=2008 |pmid=18234754 |doi=10.1056/NEJMra072367 |url=http://content.nejm.org/cgi/content/full/358/5/502 |access-date=2014-02-12 |archive-date=2010-02-12 |archive-url=https://web.archive.org/web/20100212042052/http://content.nejm.org/cgi/content/full/358/5/502 |url-status=dead }}</ref><ref>{{cite journal |author=Yokota J |title=Tumor progression and metastasis |journal=Carcinogenesis. |volume=21 |issue=3 |pages=497–503 |date=2000 |pmid=10688870 |doi=10.1093/carcin/21.3.497 |url=http://carcin.oxfordjournals.org/cgi/content/full/21/3/497
}}</ref><ref>[http://nobelprize.org/nobel_prizes/medicine/laureates/1989/press.html The Nobel Prize in Physiology or Medicine 1989] to J. Michael Bishop and Harold E. Varmus for their discovery of "the cellular origin of retroviral oncogenes".</ref>

In 1976 [[J. Michael Bishop]] and [[Harold E. Varmus]] of the [[University of California, San Francisco]] showed that oncogenes were activated proto-oncogenes, found in many organisms including humans. For this discovery Bishop and Varmus were awarded the [[Nobel Prize in Physiology or Medicine]] in 1989.<ref>[http://nobelprize.org/nobel_prizes/medicine/laureates/1989/press.html Nobel Prize in Physiology or Medicine for 1989 jointly to J. Michael Bishop and Harold E. Varmus for their discovery of "the cellular origin of retroviral oncogenes".] Press Release.</ref>

== The history of a mistake ==
The work of Bishop and Varmus corrected a long-standing error. The Nobel citation includes this explanation:
:"The term oncogene was introduced in the middle of the 1960s to denote special parts of the genetic material of certain [[viruses]]. It was believed that this part of the genetic material could direct the transformation of a normal cell into a tumor cell... The favourite theory of the time was that virus-mediated cell-to-cell transmittance of oncogenes was the origin of all forms of cancer. ''This view was later proven to be incorrect''".<ref name=Nobel>[http://www.nobelprize.org/nobel_prizes/medicine/laureates/1989/press.html 1989 Nobel Prize citation]</ref>

In fact, the [[reverse transcriptase|reverse transcription]] of the virus [[RNA]] into [[DNA]] had the effect that the oncogenes become integrated into the [[chromosome|chromosomal]] DNA in the cells. It was then found that oncogene-like material could be detected in different species throughout the animal kingdom, in fact even in simple organisms with only a few cells. Furthermore, it was shown that the gene had a fixed position in the chromosomes of a certain species, and that the gene, when it constituted part of the cellular genetic material, was divided into fragments.<ref name=Nobel/>

== Proto-oncogene ==
A '''proto-oncogene''' is a normal gene that can become an oncogene due to [[mutations]] or increased [[Gene expression|expression]]. The resultant protein can be called an '''oncoprotein'''.<ref name=Kumar20>Chapter 20 in: {{cite book |author=Mitchell, Richard Sheppard | display-authors = etal |title=Robbins basic pathology| year = 2007 |publisher=Saunders |location=Philadelphia |pages= |isbn=978-1-4160-2973-1 |oclc= |doi=}} 8th edition.</ref> Proto-oncogenes code for [[protein]]s that help to regulate [[cell growth]] and [[cell differentiation|differentiation]]. Proto-oncogenes are often involved in [[signal transduction]] and execution of [[mitosis|mitogenic]] signals, usually through their [[protein]] products. Upon ''activation'', a proto-oncogene (or its product) becomes a tumor-inducing agent, an oncogene.<ref>{{cite journal |author=Todd R. & Wong D.T. |title=Oncogenes |journal=Anticancer Res. |volume=19 |issue=6A |pages=4729–46 |year=1999 |pmid=10697588}}</ref>

=== Examples ===
The MYC gene is implicated in [[Burkitt's Lymphoma]]. This starts when a [[Translocation (genetics)|chromosomal translocation]] moves an enhancer sequence close to the MYC gene. The MYC gene codes for widely used [[transcription]] factors. When the enhancer sequence is wrongly placed, these transcription factors are produced at much higher rates. Another example of an oncogene is the [[Bcr-Abl]] gene found on the 'Philadelphia Chromosome'. This is a piece of genetic material seen in Chronic Myelogenous Leukemia, caused by the translocation of pieces from chromosomes 9 and 22. Bcr-Abl codes for a receptor tyrosine kinase, which is active, causing uncontrolled cell proliferation.

== References ==
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[[Category:Viruses]]
[[Category:Cancer]]
[[Category:Genetics]]