摘要
Objective: To determine the frequency at which the CDKN2A coding region is mutated in the atypical nevi of persons with sporadic melanoma. Design: DNA samples, isolated by laser-captured microdissection of atypical nevi from 10 patients with newly incident cases of sporadic melanoma and their spouses as matched controls, were used as templates for nested polymerase chain reaction amplification of CDKN2A exons 1 and 2. Results: No point mutations in the coding region of CDKN2A were observed in any of the melanocytic nevi. Conclusions: Point mutations in CDKN2A are an uncommon event in the atypical nevi of persons with melanoma. As such, the data may support a hypothesis of melanocytic nevus histogenesis, in which the melanocytic nevus and malignant melanoma represent separate, pleiotropic pathways resulting from common stimuli, such as genomic damage from UV radiation.
Objective: To determine the frequency at which the CDKN2A coding region is mutated in the atypical nevi of persons with sporadic melanoma. Design: DNA samples, isolated by laser-captured microdissection of atypical nevi from 10 patients with newly incident cases of sporadic melanoma and their spouses as matched controls, were used as templates for nested polymerase chain reaction amplification of CDKN2A exons 1 and 2. Results: No point mutations in the coding region of CDKN2A were observed in any of the melanocytic nevi. Conclusions: Point mutations in CDKN2A are an uncommon event in the atypical nevi of persons with melanoma. As such, the data may support a hypothesis of melanocytic nevus histogenesis, in which the melanocytic nevus and malignant melanoma represent separate, pleiotropic pathways resulting from common stimuli, such as genomic damage from UV radiation.
