致癌物
苯并(a)芘
加合物
肺癌
鸟嘌呤
化学
赫拉
癌症研究
芘
外显子
分子生物学
核苷酸
遗传学
基因
生物
生物化学
医学
病理
体外
有机化学
作者
Mikhail F. Denissenko,Annie Pao,Moon‐shong Tang,Gerd P. Pfeifer
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1996-10-18
卷期号:274 (5286): 430-432
被引量:1598
标识
DOI:10.1126/science.274.5286.430
摘要
Cigarette smoke carcinogens such as benzo[a]pyrene are implicated in the development of lung cancer. The distribution of benzo[a]pyrene diol epoxide (BPDE) adducts along exons of the P53 gene in BPDE-treated HeLa cells and bronchial epithelial cells was mapped at nucleotide resolution. Strong and selective adduct formation occurred at guanine positions in codons 157, 248, and 273. These same positions are the major mutational hotspots in human lung cancers. Thus, targeted adduct formation rather than phenotypic selection appears to shape the P53 mutational spectrum in lung cancer. These results provide a direct etiological link between a defined chemical carcinogen and human cancer.
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