期刊
SEMINARS IN CANCER BIOLOGY
卷 15, 期 2, 页码 103-112出版社
ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2004.08.005
关键词
p53 mutation spectra; polycyclic aromatic hydrocarbons; tumorigenic selection
类别
Molecular epidemiologists usually consider the spectrum of p53 mutations found in human tumors to be a signature of the corresponding environmental carcinogen(s). In lung cancer, this signature is the spectrum of G --> T transversions, presumably induced by polycyclic aromatic hydrocarbons (PAH) from cigarette smoke. What complicates the situation, however, is that in the p53 gene the same codons are preferential targets for not only mutagenesis but also tumorigenic selection. In this review, we compare the G --> T spectra induced by PAH o-quinones and diol epoxides with those in lung cancer and show that the main shaper of the latter is selection, not mutagenesis. In addition, we propose the approach that allows to distinguish selection and mutagenesis components of the p53 spectra and, therefore, to test the suspect carcinogens for their in vivo mutagenic involvement. Collectively, the reviewed basic premises, concepts and data are consistent with the increasing recognition of environmental cancer risk conditions as selecting rather than inducing tumorigenic mutations. (C) 2004 Elsevier Ltd. All rights reserved.
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