Editing Gene duplication (section)

===Role in cancer===
Duplications of [[oncogenes]] are a common cause of many types of [[cancer]]. In such cases the genetic duplication occurs in a somatic cell and affects only the genome of the cancer cells themselves, not the entire organism, much less any subsequent offspring. Recent comprehensive patient-level classification and quantification of driver events in [[The Cancer Genome Atlas|TCGA]] cohorts revealed that there are on average 12 driver events per tumor, of which 1.5 are amplifications of oncogenes.<ref>{{cite journal |last1=Vyatkin |first1=Alexey D. |last2=Otnyukov |first2=Danila V. |last3=Leonov |first3=Sergey V. |last4=Belikov |first4=Aleksey V. |title=Comprehensive patient-level classification and quantification of driver events in TCGA PanCanAtlas cohorts |journal=PLOS Genetics |date=14 January 2022 |volume=18 |issue=1 |pages=e1009996 |doi=10.1371/journal.pgen.1009996|pmid=35030162 |pmc=8759692 |doi-access=free }}</ref>

{|class="wikitable"
|+Common oncogene amplifications in human cancers
|-
! Cancer type !! Associated gene<br> amplifications !! Prevalence of <br>amplification <br>in cancer type<br> (percent)
|-
|rowspan=5| [[Breast cancer]] || [[MYC]] || 20%<ref name=Vogelstein2002>{{cite book |last1=Kinzler |first1=Kenneth W. |last2=Vogelstein |first2=Bert | name-list-style = vanc |title=The genetic basis of human cancer |publisher=McGraw-Hill |year=2002 |page=116 |isbn=978-0-07-137050-9 |url=https://books.google.com/books?id=pYG09OPbXp0C&pg=PA116 }}</ref>
|-
| [[ERBB2]] ([[HER2]]) || 20%<ref name=Vogelstein2002/>
|-
| [[CCND1]] ([[Cyclin D1]]) || 15–20%<ref name=Vogelstein2002/>
|-
| [[FGFR1]] || 12%<ref name=Vogelstein2002/>
|-
| [[FGFR2]] ||  12%<ref name=Vogelstein2002/>
|-
|rowspan=2| [[Cervical cancer]] || [[MYC]] || 25–50%<ref name=Vogelstein2002/>
|-
| [[ERBB2]] || 20%<ref name=Vogelstein2002/>
|-
|rowspan=3| [[Colorectal cancer]] || [[HRAS]] || 30%<ref name=Vogelstein2002/>
|-
| [[KRAS]] || 20%<ref name=Vogelstein2002/>
|-
| [[MYB (gene)|MYB]] || 15–20%<ref name=Vogelstein2002/>
|-
|rowspan=3| [[Esophageal cancer]] || [[MYC]] || 40%<ref name=Vogelstein2002/>
|-
| [[CCND1]] || 25%<ref name=Vogelstein2002/>
|-
| [[MDM2]] || 13%<ref name=Vogelstein2002/>
|-
|rowspan=3| [[Gastric cancer]] || [[Cyclin E|CCNE]] ([[Cyclin E]]) || 15%<ref name=Vogelstein2002/>
|-
| [[KRAS]] || 10%<ref name=Vogelstein2002/>
|-
| [[C-Met|MET]] || 10%<ref name=Vogelstein2002/>
|-
|rowspan=2| [[Glioblastoma]] || [[epidermal growth factor receptor|ERBB1]] ([[epidermal growth factor receptor|EGFR]]) || 33–50%<ref name=Vogelstein2002/>
|-
| [[CDK4]] || 15%<ref name=Vogelstein2002/>
|-
|rowspan=3| [[Head and neck cancer]] || [[CCND1]] || 50%<ref name=Vogelstein2002/>
|-
| [[epidermal growth factor receptor|ERBB1]] || 10%<ref name=Vogelstein2002/>
|-
| [[MYC]] || 7–10%<ref name=Vogelstein2002/>
|-
| [[Hepatocellular cancer]] || [[CCND1]] || 13%<ref name=Vogelstein2002/>
|-
| [[Neuroblastoma]] || [[MYCN]] || 20–25%<ref name=Vogelstein2002/>
|-
|rowspan=3| [[Ovarian cancer]] || [[MYC]] || 20–30%<ref name=Vogelstein2002/>
|-
| [[ERBB2]] || 15–30%<ref name=Vogelstein2002/>
|-
| [[AKT2]] || 12%<ref name=Vogelstein2002/>
|-
|rowspan=2| [[Sarcoma]] || [[MDM2]] || 10–30%<ref name=Vogelstein2002/>
|-
| [[CDK4]] || 10%<ref name=Vogelstein2002/>
|-
| [[Small cell lung cancer]] || [[MYC]] || 15–20%<ref name=Vogelstein2002/>
|-
|}


Whole-genome duplications are also frequent in cancers, detected in 30% to 36% of tumors from the most common cancer types.<ref>{{Cite journal |last1=Bielski |first1=Craig M. |last2=Zehir |first2=Ahmet |last3=Penson |first3=Alexander V. |last4=Donoghue |first4=Mark T. A. |last5=Chatila |first5=Walid |last6=Armenia |first6=Joshua |last7=Chang |first7=Matthew T. |last8=Schram |first8=Alison M. |last9=Jonsson |first9=Philip |last10=Bandlamudi |first10=Chaitanya |last11=Razavi |first11=Pedram |last12=Iyer |first12=Gopa |last13=Robson |first13=Mark E. |last14=Stadler |first14=Zsofia K. |last15=Schultz |first15=Nikolaus |date=2018 |title=Genome doubling shapes the evolution and prognosis of advanced cancers |journal=Nature Genetics |language=en |volume=50 |issue=8 |pages=1189–1195 |doi=10.1038/s41588-018-0165-1 |pmid=30013179 |issn=1546-1718|pmc=6072608 }}</ref><ref>{{Cite journal |last1=Quinton |first1=Ryan J. |last2=DiDomizio |first2=Amanda |last3=Vittoria |first3=Marc A. |last4=Kotýnková |first4=Kristýna |last5=Ticas |first5=Carlos J. |last6=Patel |first6=Sheena |last7=Koga |first7=Yusuke |last8=Vakhshoorzadeh |first8=Jasmine |last9=Hermance |first9=Nicole |last10=Kuroda |first10=Taruho S. |last11=Parulekar |first11=Neha |last12=Taylor |first12=Alison M. |last13=Manning |first13=Amity L. |last14=Campbell |first14=Joshua D. |last15=Ganem |first15=Neil J. |date=2021 |title=Whole-genome doubling confers unique genetic vulnerabilities on tumour cells |journal=Nature |language=en |volume=590 |issue=7846 |pages=492–497 |doi=10.1038/s41586-020-03133-3 |pmid=33505027 |issn=1476-4687|pmc=7889737 |bibcode=2021Natur.590..492Q }}</ref> Their exact role in carcinogenesis is unclear, but they in some cases lead to loss of chromatin segregation leading to chromatin conformation changes that in turn lead to oncogenic epigenetic and transcriptional modifications.<ref>{{Cite journal |last1=Lambuta |first1=Ruxandra A. |last2=Nanni |first2=Luca |last3=Liu |first3=Yuanlong |last4=Diaz-Miyar |first4=Juan |last5=Iyer |first5=Arvind |last6=Tavernari |first6=Daniele |last7=Katanayeva |first7=Natalya |last8=Ciriello |first8=Giovanni |last9=Oricchio |first9=Elisa |date=2023-03-15 |title=Whole-genome doubling drives oncogenic loss of chromatin segregation |journal=Nature |volume=615 |issue=7954 |language=en |pages=925–933 |doi=10.1038/s41586-023-05794-2 |issn=1476-4687|doi-access=free |pmid=36922594 |pmc=10060163 |bibcode=2023Natur.615..925L }}</ref>