Editing Apoptosis (section)

====Dysregulation of p53====
The tumor-suppressor protein [[p53]] accumulates when DNA is damaged due to a chain of biochemical factors. Part of this pathway includes alpha-[[interferon]] and beta-interferon, which induce transcription of the ''p53'' gene, resulting in the increase of p53 protein level and enhancement of cancer cell-apoptosis.<ref name="takaoka">{{cite journal | vauthors = Takaoka A, Hayakawa S, Yanai H, Stoiber D, Negishi H, Kikuchi H, Sasaki S, Imai K, Shibue T, Honda K, Taniguchi T | display-authors = 6 | title = Integration of interferon-alpha/beta signalling to p53 responses in tumour suppression and antiviral defence | journal = Nature | volume = 424 | issue = 6948 | pages = 516–523 | date = July 2003 | pmid = 12872134 | doi = 10.1038/nature01850 | doi-access = free | bibcode = 2003Natur.424..516T }}</ref> p53 prevents the cell from replicating by stopping the [[cell cycle]] at G1, or interphase, to give the cell time to repair; however, it will induce apoptosis if damage is extensive and repair efforts fail.<ref name="pmid12052432">{{cite journal | vauthors = Bernstein C, Bernstein H, Payne CM, Garewal H | title = DNA repair/pro-apoptotic dual-role proteins in five major DNA repair pathways: fail-safe protection against carcinogenesis | journal = Mutation Research | volume = 511 | issue = 2 | pages = 145–178 | date = June 2002 | pmid = 12052432 | doi = 10.1016/S1383-5742(02)00009-1 | bibcode = 2002MRRMR.511..145B }}</ref> Any disruption to the regulation of the ''p53'' or interferon genes will result in impaired apoptosis and the possible formation of tumors.<ref>{{Cite journal |last=Soussi |first=Thierry |date=2000 |title=The p53 Tumor Suppressor Gene: From Molecular Biology to Clinical Investigation |url=https://nyaspubs.onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2000.tb06705.x |journal=Annals of the New York Academy of Sciences |language=en |volume=910 |issue=1 |pages=121–139 |doi=10.1111/j.1749-6632.2000.tb06705.x |pmid=10911910 |bibcode=2000NYASA.910..121S |issn=1749-6632}}</ref>