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<https://discovery.ucl.ac.uk/id/eprint/10186871> <http://purl.org/dc/terms/title> "The role of p16 in senescence,  immunity and cutaneous melanoma  development"^^<http://www.w3.org/2001/XMLSchema#string> .
<https://discovery.ucl.ac.uk/id/eprint/10186871> <http://purl.org/ontology/bibo/abstract> "Melanoma is an aggressive skin cancer, approximately 3-5% of which arise from an \r\ninherited genetic mutation (Goldstein and Tucker 2001; Rossi et al. 2019), most \r\ncommonly the germline heterozygous CDKN2A mutation. The CDKN2A gene \r\nencodes p16, a tumour suppressor. Tumour suppressor mutations are known to result \r\nin increased tumours; however it is not understood why most individuals with the \r\nCDKN2A mutation mostly manifest cutaneous melanoma. In this study I aimed to \r\nexamine the cellular basis underlying excess melanomas in people with the CDKN2A \r\nmutation by examining cellular senescence and immunity. \r\nConsenting patients with the CDKN2A mutation were recruited from the NHS, and \r\nhealthy donors were recruited as controls from the public. Blood and skin biopsies \r\nwere taken for the investigation of senescence and immunity characteristics.\r\nDonors with the CDKN2A mutation exhibit altered cutaneous senescence features, \r\nspecifically CDKN2A-melanocytes express less p16 and have fewer telomere \r\nassociated foci (TAF) than control melanocytes. CDKN2A-melanocytes and \r\nfibroblasts can be induced to senescence; however CDKN2A-fibroblasts display\r\ndelayed replicative senescence when compared to control fibroblasts. When \r\nconsidering immunity, healthy CDKN2A-skin exhibits reduced numbers of T cells \r\nwhen compared to control skin. Patient skin also shows diminished expression of \r\nMelan A, a protein exclusively expressed by melanocytes. Cytometric bead array \r\nstudies in vitro show cutaneous ‘senescent’ fibroblasts from CDKN2A-donors produce \r\nless leucocyte chemoattractants (CXCL10, CCL5, IL6) than controls. \r\nThe germline human CDKN2A-mutation confers a multi-layered deficit underlying the \r\npropensity to cutaneous melanoma. Baseline senescence dysregulation likely lowers \r\nthe threshold for total loss of senescence through ultraviolet radiation-induced DNA \r\ndamage. The altered chemoattractant secretion from CDKN2A-fibroblasts could result \r\nin the recruitment of fewer lymphocytes into the skin of patients at basal steady-state. \r\nMoreover, the specific reduction of Melan A, a key antigen in activating anti melanocyte cytotoxicity, alongside reduced lymphocyte numbers could impair destruction of melanocytes in the early stages of tumour formation. These findings suggest potential treatment avenues for people with the CDKN2A mutation, including Melan A vaccination to boost anti-melanocyte antigenicity."^^<http://www.w3.org/2001/XMLSchema#string> .
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