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Here, using genetically engineered mouse models, we demonstrate that\n                    <jats:italic>Kmt2c<\/jats:italic>\n                    \/\n                    <jats:italic>d<\/jats:italic>\n                    knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and\n                    <jats:italic>Kmt2c<\/jats:italic>\n                    \/\n                    <jats:italic>d<\/jats:italic>\n                    knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation.\n                    <jats:italic>Kmt2c<\/jats:italic>\n                    \/\n                    <jats:italic>d<\/jats:italic>\n                    knockout further led to KMT2A\u2013menin redistribution from KMT2D localized enhancers to CpG-high and bivalent promoters, resulting in derepression of signal-induced immediate early genes. Therapeutically,\n                    <jats:italic>Kmt2c<\/jats:italic>\n                    <jats:italic>\/<\/jats:italic>\n                    <jats:italic>d<\/jats:italic>\n                    knockout upregulated epidermal growth factor receptor signaling and conferred vulnerability to epidermal growth factor receptor inhibitors. Together, our data posit that functional loss of\n                    <jats:italic>Kmt2c<\/jats:italic>\n                    \/\n                    <jats:italic>d<\/jats:italic>\n                    licenses a molecular \u2018field effect\u2019 priming histologically normal urothelium for oncogenic transformation and presents therapeutic vulnerabilities.\n                  <\/jats:p>","DOI":"10.1038\/s41588-024-02015-y","type":"journal-article","created":{"date-parts":[[2025,1,13]],"date-time":"2025-01-13T05:04:05Z","timestamp":1736744645000},"page":"165-179","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Loss of Kmt2c or Kmt2d primes urothelium for tumorigenesis and redistributes KMT2A\u2013menin to bivalent promoters"],"prefix":"10.1038","volume":"57","author":[{"given":"Naitao","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohini R.","family":"Pachai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8777-4580","authenticated-orcid":false,"given":"Dan","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cindy J.","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8067-8804","authenticated-orcid":false,"given":"Sarah","family":"Warda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Makhzuna N.","family":"Khudoynazarova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-6451-8996","authenticated-orcid":false,"given":"Woo Hyun","family":"Cho","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guojia","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sagar R.","family":"Shah","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2827-8824","authenticated-orcid":false,"given":"Li","family":"Yao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheng","family":"Qian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elissa W. 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P.C. has received institutional research funding from Pfizer\/Array, Novartis, Deciphera and Ningbo NewBay Medical Technology. Y.C. has stock ownership and received royalties from Oric Pharmaceuticals. S.C. has received institutional research support from Daiichi-Sankyo, Paige.ai and AstraZeneca, is founder\/shareholder of Odyssey Biosciences, has shares in Totus Medicines, and personal consulting fees from Sanofi, Novartis, Inivata, Lilly and AstraZeneca. J.E.R. has received personal honoraria\/consulting fees from BMS, Merck, Pfizer, Pharmacyclics, Boheringer Ingelheim, EMD-Serono, GSK, Infinity, Janssen, Mirati, BioClin, Lilly, Tyra Biosciences, Astellas, Seagen, Bayer, AstraZeneca, Roche\/Genentech and QED Therapeutics, and conducted trials from Astellas, Seagen, Bayer, AstraZeneca, Roche\/Genentech and QED Therapeutics. S.R.S. is an equity holder and member of the scientific advisory board of NeuScience, Inc. and a consultant at Third Bridge Group Limited. D.B.S. has consulted\/received honoraria from Rain, Pfizer, Fog Pharma, PaigeAI, BridgeBio, Scorpion Therapeutics, FORE Therapeutics, Function Oncology, Pyramid and Elsie Biotechnologies, Inc. None of these disclosures are directly related to this study. The other authors declare no competing interests.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}]}}