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Immune responses are known to select (immunoedit) tumour cells displaying immunoevasive properties. Here we address the role of IFN-\u03b3 in mediating the immunoediting process. We observe that, in several mouse tumour models such as HA-expressing 4T1 mammary carcinoma cells, OVA-expressing EG7 lymphoma cells and CMS5 MCA-induced fibrosarcoma cells naturally expressing mutated extracellular signal-regulated kinase (ERK) antigen, the action of antigen-specific cytotoxic T cell (CTL) <jats:italic>in vivo<\/jats:italic> results in the emergence of resistant cancer cell clones only in the presence of IFN-\u03b3 within the tumour microenvironment. Moreover, we show that exposure of tumours to IFN-\u03b3-producing antigen-specific CTLs <jats:italic>in vivo<\/jats:italic> results in copy-number alterations (CNAs) associated with DNA damage response and modulation of DNA editing\/repair gene expression. These results suggest that enhanced genetic instability might be one of the mechanisms by which CTLs and IFN-\u03b3 immunoedits tumours, altering their immune resistance as a result of genetic evolution.<\/jats:p>","DOI":"10.1038\/ncomms14607","type":"journal-article","created":{"date-parts":[[2017,2,24]],"date-time":"2017-02-24T10:05:25Z","timestamp":1487930725000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":147,"title":["IFN-\u03b3 is required for cytotoxic T cell-dependent cancer genome immunoediting"],"prefix":"10.1038","volume":"8","author":[{"given":"Kazuyoshi","family":"Takeda","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masafumi","family":"Nakayama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihiro","family":"Hayakawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuko","family":"Kojima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroaki","family":"Ikeda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naoko","family":"Imai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kouetsu","family":"Ogasawara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ko","family":"Okumura","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M.","family":"Thomas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark J.","family":"Smyth","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,2,24]]},"reference":[{"key":"BFncomms14607_CR1","doi-asserted-by":"publisher","first-page":"1565","DOI":"10.1126\/science.1203486","volume":"331","author":"RD Schreiber","year":"2011","unstructured":"Schreiber, R. 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