dc.contributor.author | Prime, SS | |
dc.contributor.author | Darski, P | |
dc.contributor.author | Hunter, KD | |
dc.contributor.author | Cirillo, N | |
dc.contributor.author | Parkinson, EK | |
dc.date.accessioned | 2024-07-31T14:31:21Z | |
dc.date.available | 2024-04-01 | |
dc.date.available | 2024-07-31T14:31:21Z | |
dc.date.issued | 2024-04-07 | |
dc.identifier.citation | Prime, S.S.; Darski, P.; Hunter, K.D.; Cirillo, N.; Parkinson, E.K. A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer. Int. J. Mol. Sci. 2024, 25, 4092. https://doi.org/10.3390/ijms25074092 | en_US |
dc.identifier.uri | https://qmro.qmul.ac.uk/xmlui/handle/123456789/98523 | |
dc.description.abstract | 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's 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. | en_US |
dc.language | eng | |
dc.publisher | MDPI | en_US |
dc.relation.ispartof | Int J Mol Sci | |
dc.rights | This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). | |
dc.subject | DNA repair | en_US |
dc.subject | Fanconi anemia | en_US |
dc.subject | double strand breaks | en_US |
dc.subject | homologous recombination | en_US |
dc.subject | non-homologous end joining | en_US |
dc.subject | oral cancer development | en_US |
dc.subject | Humans | en_US |
dc.subject | Mouth Neoplasms | en_US |
dc.subject | Carcinoma, Squamous Cell | en_US |
dc.subject | Squamous Cell Carcinoma of Head and Neck | en_US |
dc.subject | Fanconi Anemia | en_US |
dc.subject | Head and Neck Neoplasms | en_US |
dc.subject | DNA | en_US |
dc.title | A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer. | en_US |
dc.type | Article | en_US |
dc.rights.holder | © 2024 by the authors. Licensee MDPI, Basel, Switzerland. | |
dc.identifier.doi | 10.3390/ijms25074092 | |
pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/38612901 | en_US |
pubs.issue | 7 | en_US |
pubs.notes | Not known | en_US |
pubs.publication-status | Published online | en_US |
pubs.volume | 25 | en_US |
dcterms.dateAccepted | 2024-04-01 | |
rioxxterms.funder | Default funder | en_US |
rioxxterms.identifier.project | Default project | en_US |
rioxxterms.funder.project | b215eee3-195d-4c4f-a85d-169a4331c138 | en_US |