Repair of directly and indirectly UV-induced DNA lesions and of DNA double-strand breaks in cells from skin cancer-prone patients with the disorders dysplastic nevus syndrome or basal cell nevus syndrome.

Abstract

Hereditary disorders carrying an increased skin cancer risk, such as xeroderma pigmentosum (XP), dysplastic nevus syndrome (DNS), or basal cell nevus syndrome (BCNS), are valuable model systems that might provide insights into general mechanisms of skin carcinogenesis. This is especially true of XP, in which a defective repair of UV-induced DNA damage explains the increased risk of basal cell carcinomas, squamous cell carcinomas, and malignant melanomas in UV-exposed skin of affected patients (Kraemer et al. 1987; Barnes et al. 1993; Hoijmakers 1993).KeywordsBasal Cell CarcinomaXeroderma PigmentosumLinear PlasmidNormal Cell LineNevoid Basal Cell Carcinoma SyndromeThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.