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The \u2018Y-family\u2019 trans-lesion synthesis (TLS) DNA polymerases enable cells to replicate damaged genomes, thereby conferring DNA damage tolerance. Moreover, Y-family DNA polymerases are inherently error-prone and cause mutations. Therefore, TLS DNA polymerases are potential mediators of important tumorigenic phenotypes. The skin cancer-propensity syndrome xeroderma pigmentosum-variant (XPV) results from defects in the Y-family DNA Polymerase Pol eta (Pol\u03b7) and compensatory deployment of alternative inappropriate DNA polymerases. However, the extent to which dysregulated TLS contributes to the underlying etiology of other human cancers is unclear. Here we consider the broad impact of TLS polymerases on tumorigenesis and cancer therapy. We survey the ways in which TLS DNA polymerases are pathologically altered in cancer. We summarize evidence that TLS polymerases shape cancer genomes, and review studies implicating dysregulated TLS as a driver of carcinogenesis. Because many cancer treatment regimens comprise DNA-damaging agents, pharmacological inhibition of TLS is an attractive strategy for sensitizing tumors to genotoxic therapies. Therefore, we discuss the pharmacological tractability of the TLS pathway and summarize recent progress on development of TLS inhibitors for therapeutic purposes.<\/jats:p>","DOI":"10.1093\/narcan\/zcad005","type":"journal-article","created":{"date-parts":[[2023,2,6]],"date-time":"2023-02-06T04:11:47Z","timestamp":1675656707000},"source":"Crossref","is-referenced-by-count":80,"title":["Roles of trans-lesion synthesis (TLS) DNA polymerases in tumorigenesis and cancer therapy"],"prefix":"10.1093","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2071-9891","authenticated-orcid":false,"given":"Jay","family":"Anand","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill , 614 Brinkhous-Bullitt Building, Chapel Hill, NC 27599, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lilly","family":"Chiou","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill , 614 Brinkhous-Bullitt Building, Chapel Hill, NC 27599, USA"},{"name":"Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill , Chapel Hill, NC 27599, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carly","family":"Sciandra","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Duke University School of Medicine , Durham , NC 27710, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingyuan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of North Carolina at Chapel Hill , 135 Dauer Drive , 3101 McGavran-Greenberg Hall, Chapel Hill, NC 27599, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiyong","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Chemistry, Duke University , Durham , NC 27708, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8331-2357","authenticated-orcid":false,"given":"Di","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of North Carolina at Chapel Hill , 135 Dauer Drive , 3101 McGavran-Greenberg Hall, Chapel Hill, NC 27599, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pei","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Duke University School of Medicine , Durham , NC 27710, USA"}],"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 , 614 Brinkhous-Bullitt Building, Chapel Hill, NC 27599, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,2,6]]},"reference":[{"key":"2024032321000028900_B1","doi-asserted-by":"crossref","first-page":"57","DOI":"10.1016\/S0092-8674(00)81683-9","article-title":"The hallmarks of cancer","volume":"100","author":"Hanahan","year":"2000","journal-title":"Cell"},{"key":"2024032321000028900_B2","doi-asserted-by":"crossref","first-page":"646","DOI":"10.1016\/j.cell.2011.02.013","article-title":"Hallmarks of cancer: the next generation","volume":"144","author":"Hanahan","year":"2011","journal-title":"Cell"},{"key":"2024032321000028900_B3","doi-asserted-by":"crossref","first-page":"74","DOI":"10.1016\/S0968-0004(99)01524-8","article-title":"Lesions in DNA: hurdles for polymerases","volume":"25","author":"Baynton","year":"2000","journal-title":"Trends Biochem. Sci."},{"key":"2024032321000028900_B4","doi-asserted-by":"crossref","first-page":"640","DOI":"10.1038\/ncb1417","article-title":"the Y-family DNA polymerase kappa (pol kappa) functions in mammalian nucleotide-excision repair","volume":"8","author":"Ogi","year":"2006","journal-title":"Nat. Cell Biol."},{"key":"2024032321000028900_B5","doi-asserted-by":"crossref","first-page":"714","DOI":"10.1016\/j.molcel.2010.02.009","article-title":"Three DNA polymerases, recruited by different mechanisms, carry out NER repair synthesis in human cells","volume":"37","author":"Ogi","year":"2010","journal-title":"Mol. 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