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This study identifies previously unrecognized recurrent activating mutations in the G9a histone methyltransferase gene, as well as G9a genomic copy gains in approximately 26% of human melanomas, which collectively drive tumor growth and an immunologically sterile microenvironment beyond melanoma. Furthermore, the WNT pathway is identified as a key tumorigenic target of G9a gain-of-function, via suppression of the WNT antagonist DKK1. Importantly, genetic or pharmacologic suppression of mutated or amplified G9a using multiple in vitro and in vivo models demonstrates that G9a is a druggable target for therapeutic intervention in melanoma and other cancers harboring G9a genomic aberrations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>Oncogenic G9a abnormalities drive tumorigenesis and the \u201ccold\u201d immune microenvironment by activating WNT signaling through DKK1 repression. These results reveal a key druggable mechanism for tumor development and identify strategies to restore \u201chot\u201d tumor immune microenvironments.<\/jats:p>\n                    <jats:p>This article is highlighted in the In This Issue feature, p. 890<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/2159-8290.cd-19-0532","type":"journal-article","created":{"date-parts":[[2020,4,8]],"date-time":"2020-04-08T14:05:19Z","timestamp":1586354719000},"page":"980-997","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":64,"title":["Gain-of-Function Genetic Alterations of G9a Drive Oncogenesis"],"prefix":"10.1158","volume":"10","author":[{"given":"Shinichiro","family":"Kato","sequence":"first","affiliation":[{"name":"1Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Charlestown, 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