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RAD18 is also frequently overexpressed and pathologically activated in cancer cells. However, the extent to which RAD18 shapes cancer genomes and impacts tumorigenesis is unclear. Therefore, we tested the effect of Rad18 status on chemically induced and oncogene-driven tumorigenesis. In a chemically induced oral carcinogenesis model, acute (2\u201316 days) 4NQO treatment induces expression of Rad18 and TLS polymerase mRNAs in mouse oral epithelial cells prior to the emergence of oral squamous cell carcinomas (OSCCs). Chronic (8-week) 4NQO treatment leads to the onset of oral tumors that is accelerated in\u00a0Rad18\u2212\/\u2212 mice when compared with Rad18+\/+ animals. Analysis of OSCC exomes reveals increased levels of G(C)&amp;gt;T(A) transversions in Rad18\u2212\/\u2212 tumors when compared with Rad18+\/+. Therefore, Rad18 promotes error-free bypass of 4NQO-induced DNA lesions and suppresses 4NQO-induced oral carcinogenesis. In a KrasG12D-induced lung carcinogenesis model, Rad18 deficiency did not affect rates or incidence of oncogene-induced lung tumors or mutations. Taken together, we demonstrate that Rad18 has context-specific tumor-suppressive activity. Given the prevalence of 4NQO-like environmental exposures, RAD18 is highly likely to shape human cancer genomes and perhaps influence other aspects of the tumorigenic process.<\/jats:p>","DOI":"10.1093\/narcan\/zcag001","type":"journal-article","created":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T12:46:35Z","timestamp":1767789995000},"source":"Crossref","is-referenced-by-count":2,"title":["Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesis\u00a0\n                    <i>in vivo<\/i>"],"prefix":"10.1093","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2071-9891","authenticated-orcid":false,"given":"Jay R","family":"Anand","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bethany Wagner","family":"Brown","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jitong","family":"Lou","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qisheng","family":"Gu","sequence":"additional","affiliation":[{"name":"Division of Oral and Craniofacial Health Sciences, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill , Chapel 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Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United States"]},{"name":"Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cyrus","family":"Vaziri","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United States"]},{"name":"Curriculum in Genetics and Molecular Biology, University of North Carolina , Chapel Hill, NC 27599 ,","place":["United States"]},{"name":"Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599 ,","place":["United 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