Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer.
Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer.
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DOI：
10.1016/0168-9525(94)90251-8
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发表时间：
1994-03
期刊：
影响因子：
56.9
通讯作者：
Silvia Tornaletti;Gerd P. Pfeifer
中科院分区：
文献类型：
--
作者：
Silvia Tornaletti;Gerd P. Pfeifer
紫外线与人类皮肤癌的发生有关。这类癌症通常表现为p53肿瘤抑制基因的突变。采用连接介导的聚合酶链反应，在核苷酸分辨率上分析了环丁烷嘧啶二聚体沿p53基因的修复。单个核苷酸的修复率是高度可变和序列依赖的。在皮肤癌中经常发生突变的8个位置中，有7个位置的修复速度较慢，这表明修复效率可能与癌症相关基因的突变谱有很大关系。
Ultraviolet light has been linked with the development of human skin cancers. Such cancers often exhibit mutations in thep53tumor suppressor gene. Ligation-mediated polymerase chain reaction was used to analyze at nucleotide resolution the repair of cyclobutane pyrimidine dimers along thep53gene in ultraviolet-irradiated human fibroblasts. Repair rates at individual nucleotides were highly variable and sequence-dependent. Slow repair was seen at seven of eight positions frequently mutated in skin cancer, suggesting that repair efficiency may strongly contribute to the mutation spectrum in a cancer-associated gene.