Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Oncogene
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
{{Short description|Gene that has the potential to cause cancer}} {{For|the journal|Oncogene (journal)}} [[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 and Tumor Suppressor Genes">{{cite book | veditors = Wilbur B |title = The World of the Cell | edition = 7th | location = San Francisco, California | year = 2009 }}</ref> In [[tumor]] [[Cell (biology)|cells]], these genes are often [[mutated]], or [[Gene expression|expressed]] at high levels.<ref name="Kimball's Biology Pages">[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 preprogrammed rapid cell death ([[apoptosis]]) if critical functions are altered and then malfunction. 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 began as proto-oncogenes: normal genes involved in cell growth and proliferation or inhibition of apoptosis. If, through mutation, normal genes promoting cellular growth are up-regulated (gain-of-function mutation), they predispose the cell to cancer and are termed ''oncogenes''. Usually, multiple oncogenes, along with mutated apoptotic or [[Tumor suppressor gene|tumor suppressor genes]], act in concert to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the [[protein]]s encoded by oncogenes.<ref name="Kimball's Biology Pages"/><ref>{{cite journal | vauthors = Croce CM | title = Oncogenes and cancer | journal = The New England Journal of Medicine | volume = 358 | issue = 5 | pages = 502–511 | date = January 2008 | pmid = 18234754 | doi = 10.1056/NEJMra072367 }}</ref><ref>{{cite journal | vauthors = Yokota J | title = Tumor progression and metastasis | journal = Carcinogenesis | volume = 21 | issue = 3 | pages = 497–503 | date = March 2000 | pmid = 10688870 | doi = 10.1093/carcin/21.3.497 | doi-access = free }}</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> Oncogenes are a physically and functionally diverse set of genes, and as a result, their protein products have [[pleiotropic]] effects on a variety of intricate regulatory cascades within the cell. Genes known as proto-oncogenes are those that normally encourage cell growth and division in order to generate new cells or sustain the viability of pre-existing cells. When overexpressed, proto-oncogenes can be inadvertently activated (turned on), which changes them to oncogenes.<ref>{{Citation |last1=Niederhuber |first1=John E. |title=Dedication |date=2020 |url=http://dx.doi.org/10.1016/b978-0-323-47674-4.00126-2 |work=Abeloff's Clinical Oncology |pages=v |access-date=2023-12-10 |publisher=Elsevier |last2=Armitage |first2=James O. |last3=Doroshow |first3=James H. |last4=Kastan |first4=Michael B. |last5=Tepper |first5=Joel E.|doi=10.1016/b978-0-323-47674-4.00126-2 |isbn=9780323476744 |url-access=subscription }}</ref> There are numerous ways to activate (turn on) oncogenes in cells: Gene changes or mutations: A person's genetic "coding" may differ in a way that causes an oncogene to always be activated. These types of gene changes can develop spontaneously throughout the course of a person's life or they might be inherited from a parent when a [[Transcription (biology)|transcription]] error occurs during cell division.<ref>{{Cite journal |last1=Adler Jaffe |first1=Shoshana |last2=Jacobson |first2=Kendal |last3=Farnbach Pearson |first3=Amy W. |last4=Baca |first4=Lila A. |last5=Dimauro |first5=Nina |last6=Kano |first6=Miria |date=2023-05-05 |title="Did I get into the twilight zone somehow?": sexual and gender minority cancer caregiver experiences during COVID |url=http://dx.doi.org/10.1007/s10552-023-01708-9 |journal=Cancer Causes & Control |volume=34 |issue=7 |pages=563–568 |doi=10.1007/s10552-023-01708-9 |pmid=37145262 |pmc=10161178 |issn=0957-5243}}</ref> Cells can frequently switch genes on or off via epigenetic mechanisms rather than actual genetic alterations. Alternately, different chemical compounds that can be linked to genetic material (DNA or RNA) may have an impact on which genes are active. An oncogene may sporadically become activated due to these epigenetic modifications. Chromosomal rearrangement: Every living creature has chromosomes, which are substantial strands of [[DNA]] that contain the genes for a cell. A chromosome's DNA sequence may alter each time a cell divides. This could cause a gene to be located near to a proto-oncogene that acts as an "on" switch, keeping it active even when it shouldn't. The cell can develop irregularly with the aid of this new oncogene.<ref>{{Citation |last1=Teh |first1=Bin Tean |title=Genetic and Epigenetic Alterations in Cancer |date=2020 |url=http://dx.doi.org/10.1016/b978-0-323-47674-4.00014-1 |work=Abeloff's Clinical Oncology |pages=209–224.e2 |access-date=2023-12-10 |publisher=Elsevier |last2=Fearon |first2=Eric R.|doi=10.1016/b978-0-323-47674-4.00014-1 |isbn=9780323476744 |url-access=subscription }}</ref> Gene duplication: If one cell has more copies of a gene than another, that cell may produce too much of a certain protein. The first human oncogene (HRAS), a crucial finding in the field of cancer research, was discovered more than 40 years ago, and since then, the number of novel pathogenic oncogenes has increased steadily. The discovery of specific small-molecule inhibitors that specifically target the different oncogenic proteins and a comprehensive mechanistic analysis of the ways in which oncogenes dysregulate physiological signaling to cause different cancer types and developmental syndromes are potential future advances in the field of cancer research. Investigating the quickly expanding field of oncogene molecular research, the goal of this special issue was to generate practical translational indicators that could be able to meet clinical needs.<ref>{{Cite journal |last1=Chen |first1=Qiongfeng |last2=Jin |first2=Jingguang |last3=Guo |first3=Wenhui |last4=Tang |first4=Zhimin |last5=Luo |first5=Yunfei |last6=Ying |first6=Ying |last7=Lin |first7=Hui |last8=Luo |first8=Zhijun |date=2022-08-08 |title=PEBP4 Directs the Malignant Behavior of Hepatocellular Carcinoma Cells via Regulating mTORC1 and mTORC2 |journal=International Journal of Molecular Sciences |language=en |volume=23 |issue=15 |pages=8798 |doi=10.3390/ijms23158798 |pmid=35955931 |pmc=9369291 |issn=1422-0067 |doi-access=free }}</ref> Genes that are considered crucial for cancer can be divided into two categories based on whether the harmful mutations in them result in function loss or gain. Gain-of-function mutations of proto-oncogenes drive cells to proliferate when they shouldn't, while loss-of-function mutations of tumor suppressor genes free cells from inhibitions that typically serve to control their numbers. The ability of the mutant genes, known as oncogenes, to steer a specific line of test cells toward malignant proliferation can occasionally be used to identify these later mutations, which have a dominating effect. Many of them were initially found to induce cancer in animals when they are introduced through viral vector infection, which carries genetic information from a prior host cell. Another method for identifying oncogenes is to look for genes that are activated by mutations in human cancer cells or by chromosomal translocations that may indicate the presence of a gene that is crucial for cancer.<ref>{{Cite journal |last1=Abuasaker |first1=Baraa |last2=Garrido |first2=Eduardo |last3=Vilaplana |first3=Marta |last4=Gómez-Zepeda |first4=Jesús Daniel |last5=Brun |first5=Sonia |last6=Garcia-Cajide |first6=Marta |last7=Mauvezin |first7=Caroline |last8=Jaumot |first8=Montserrat |last9=Pujol |first9=Maria Dolors |last10=Rubio-Martínez |first10=Jaime |last11=Agell |first11=Neus |date=2023-01-01 |title=α4-α5 Helices on Surface of KRAS Can Accommodate Small Compounds That Increase KRAS Signaling While Inducing CRC Cell Death |journal=International Journal of Molecular Sciences |language=en |volume=24 |issue=1 |pages=748 |doi=10.3390/ijms24010748 |pmid=36614192 |issn=1422-0067 |doi-access=free |pmc=9821572 }}</ref> Cancer patients are generally categorized according to clinical parameters in order to tailor their [[Cancer treatment|cancer therapy]]. For example, the separation of patients with [[acute leukemia]] into those with [[lymphocytic leukemia]] and those with [[Myeloid leukemia|myelocytic leukemia]] is important, because the optimal treatment for each form is different. Even in a particular disease, the identification of patients with good and poor [[Prognosis|prognostic]] potential is helpful, since more aggressive therapy may be needed to achieve a cure in the poor prognostic group. Oncogenes are [[Prognosis marker|prognostic markers]] in certain human cancers. [[N-Myc|N-myc]] amplification is an independent determinant in predicting a poor outcome in childhood [[neuroblastoma]]. Those children with amplification of N-myc, regardless of stage, will have shortened survival. Thus, therapeutic efforts are concentrated on intensifying treatment in this poor prognostic group.<ref>{{Citation |last1=Larrick |first1=James W. |title=Therapeutic applications of oncogenes |date=1989 |url=http://link.springer.com/10.1007/978-1-4613-1599-5_14 |work=Oncogenes |volume=47 |pages=319–330 |editor-last=Benz |editor-first=Christopher |access-date=2023-12-10 |place=Boston, MA |publisher=Springer US |doi=10.1007/978-1-4613-1599-5_14 |isbn=978-1-4612-8885-5 |last2=Liu |first2=Edison |pmid=2577004 |editor2-last=Liu |editor2-first=Edison|url-access=subscription }}</ref>
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)