Origins and selection of p53 mutations in lung carcinogenesis.

摘要: Molecular epidemiologists usually consider the spectrum of p53 mutations found in human tumors to be a signature corresponding environmental carcinogen(s). In lung cancer, this is G → T transversions, presumably induced by polycyclic aromatic hydrocarbons (PAH) from cigarette smoke. What complicates situation, however, that gene same codons are preferential targets for not only mutagenesis but also tumorigenic selection. review, we compare spectra PAH o-quinones and diol epoxides with those cancer show main “shaper” latter selection, mutagenesis. addition, propose approach allows distinguish selection components and, therefore, test suspect carcinogens their “in vivo” mutagenic involvement. Collectively, reviewed basic premises, concepts data consistent increasing recognition risk conditions as selecting rather than inducing mutations.