{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T13:41:04Z","timestamp":1791812464334,"version":"4.3.4"},"reference-count":155,"publisher":"MDPI AG","issue":"7","license":[{"start":{"date-parts":[[2024,4,7]],"date-time":"2024-04-07T00:00:00Z","timestamp":1712448000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>We explore the possibility that defects in genes associated with the response and repair of DNA double strand breaks predispose oral potentially malignant disorders (OPMD) to undergo malignant transformation to oral squamous cell carcinoma (OSCC). Defects in the homologous recombination\/Fanconi anemia (HR\/FA), but not in the non-homologous end joining, causes the DNA repair pathway to appear to be consistent with features of familial conditions that are predisposed to OSCC (FA, Bloom\u2019s syndrome, Ataxia Telangiectasia); this is true for OSCC that occurs in young patients, sometimes with little\/no exposure to classical risk factors. Even in Dyskeratosis Congenita, a disorder of the telomerase complex that is also predisposed to OSCC, attempts at maintaining telomere length involve a pathway with shared HR genes. Defects in the HR\/FA pathway therefore appear to be pivotal in conditions that are predisposed to OSCC. There is also some evidence that abnormalities in the HR\/FA pathway are associated with malignant transformation of sporadic cases OPMD and OSCC. We provide data showing overexpression of HR\/FA genes in a cell-cycle-dependent manner in a series of OPMD-derived immortal keratinocyte cell lines compared to their mortal counterparts. The observations in this study argue strongly for an important role of the HA\/FA DNA repair pathway in the development of OSCC.<\/jats:p>","DOI":"10.3390\/ijms25074092","type":"journal-article","created":{"date-parts":[[2024,4,8]],"date-time":"2024-04-08T10:11:55Z","timestamp":1712571115000},"page":"4092","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer"],"prefix":"10.3390","volume":"25","author":[{"given":"Stephen S.","family":"Prime","sequence":"first","affiliation":[{"name":"Centre for Immunology and Regenerative Medicine, Institute of Dentistry, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 4NS, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6339-4260","authenticated-orcid":false,"given":"Piotr","family":"Darski","sequence":"additional","affiliation":[{"name":"Liverpool Head and Neck Centre, Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool L69 3BX, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keith D.","family":"Hunter","sequence":"additional","affiliation":[{"name":"Liverpool Head and Neck Centre, Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool L69 3BX, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1429-1323","authenticated-orcid":false,"given":"Nicola","family":"Cirillo","sequence":"additional","affiliation":[{"name":"Melbourne Dental School, University of Melbourne, 720 Swanson Street, Carlton, Melbourne, VIC 3053, Australia"},{"name":"School of Dentistry, University of Jordan, Amman 11942, Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4234-1658","authenticated-orcid":false,"given":"E. Kenneth","family":"Parkinson","sequence":"additional","affiliation":[{"name":"Centre for Immunology and Regenerative Medicine, Institute of Dentistry, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 4NS, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,4,7]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"209","DOI":"10.3322\/caac.21660","article-title":"Global statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries","volume":"71","author":"Sung","year":"2021","journal-title":"CA Cancer J. Clin."},{"key":"ref_2","unstructured":"GBD 2019 Lip, Oral and Pharyngeal Cancer Collaborators (2023). The global, regional, and national burden of adult lip, oral, and pharyngeal cancer in 204 countries and territories: A systematic analysis for the global burden of disease study 2019. 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