BACKGROUND: Non-melanoma skin cancer represents a significant cause of morbidity and mortality among renal transplant recipients. Established risk factors that increase susceptibility to skin cancer after transplantation include skin type, sun exposure and level of immunosuppression. METHODS: A comprehensive literature review was carried out to discuss relevant genetic polymorphism for the development of skin cancer in organ transplant recipients. These include genetic polymorphisms in glutathione S-transferase, interleukin-10, retinoblastoma and p53 genes. We also discuss genetic polymorphisms in the folate pathway, melanocortin 1 receptor and vitamin D receptor recently discovered in our group. RESULTS: No single factor is causative in cutaneous carcinogenesis in transplant recipients. Interactions of some of the above mechanisms with known environmental factors lead to increased risk. CONCLUSION: Polymorphisms in methylenetetrahydrofolate reductase are potentially correctable with folic acid supplementation; however, further evaluation is required in adequately powered prospective clinical trials. Avoidance of known oncogenic environmental factors and genetic risk evaluation may improve outcomes in transplant patients.
BACKGROUND:Non-melanoma skin cancer represents a significant cause of morbidity and mortality among renal transplant recipients. Established risk factors that increase susceptibility to skin cancer after transplantation include skin type, sun exposure and level of immunosuppression. METHODS: A comprehensive literature review was carried out to discuss relevant genetic polymorphism for the development of skin cancer in organ transplant recipients. These include genetic polymorphisms in glutathione S-transferase, interleukin-10, retinoblastoma and p53 genes. We also discuss genetic polymorphisms in the folate pathway, melanocortin 1 receptor and vitamin D receptor recently discovered in our group. RESULTS: No single factor is causative in cutaneous carcinogenesis in transplant recipients. Interactions of some of the above mechanisms with known environmental factors lead to increased risk. CONCLUSION: Polymorphisms in methylenetetrahydrofolate reductase are potentially correctable with folic acid supplementation; however, further evaluation is required in adequately powered prospective clinical trials. Avoidance of known oncogenic environmental factors and genetic risk evaluation may improve outcomes in transplant patients.