Several studies have shown that sun exposure, photo irradiation and ionising irradiation play a major role in the pathogenesis of SCC. DNA damage is a fundamental process that occurs in the development of cancer. Both UV light and ionising radiation are potent mutagens. Specifically, UVB light has been shown to produce pyrimidine dimers in DNA; these result in DNA point mutations during keratinocyte replication, which lead to abnormal cell function and replication.
In addition to direct DNA damage, genes involved in DNA repair have been implicated in the pathogenesis of SCC. The p53 gene is mutated in most SCC cases, disabling normal p53 function, which is thought to be critical in suppressing the development of SCC by repairing of UV-damaged DNA.17-20 Keratinocytes with p53 mutations cannot repair the mutations induced by irradiation and subsequently proliferate to develop cancer.17 Furthermore, mice with p53 mutations develop skin tumours more readily. Mutations in p53 can either be acquired (through multiple pathways including human papillomavirus, UV light, carcinogens) or inherited. People with xeroderma pigmentosum have a defective p53 pathway and develop numerous skin cancers; they cannot repair mutations induced by irradiation.21
Immunological status has also been implicated in the development of SCC. The rate of SCC in transplant recipients is high, particularly in those with a kidney or heart transplant.22-25 How immunosuppression increases the risk is not known, but decreasing the immunosuppressive therapy helps to reduce the number of SCCs. Further studies are needed to determine how altered immune responses influence the development of SCC.
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