Wang Hao, Presland Richard B, Piepkorn Michael
Department of Medicine, Division of Dermatology, University of Washington, Seattle 98195, USA.
Arch Dermatol. 2005 Feb;141(2):177-80. doi: 10.1001/archderm.141.2.177.
To determine the frequency at which the CDKN2A coding region is mutated in the atypical nevi of persons with sporadic melanoma.
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.
No point mutations in the coding region of CDKN2A were observed in any of the melanocytic nevi.
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.
确定散发型黑色素瘤患者非典型痣中CDKN2A编码区的突变频率。
通过激光捕获显微切割从10例新发病例的散发型黑色素瘤患者及其作为匹配对照的配偶的非典型痣中分离出DNA样本，用作CDKN2A外显子1和2的巢式聚合酶链反应扩增的模板。
在任何黑素细胞痣中均未观察到CDKN2A编码区的点突变。
CDKN2A中的点突变在黑色素瘤患者的非典型痣中是不常见的事件。因此，这些数据可能支持黑素细胞痣组织发生的假说，其中黑素细胞痣和恶性黑色素瘤代表由共同刺激（如紫外线辐射引起的基因组损伤）导致的不同的多效性途径。
