Mutagenesis, Vol. 17, No. 4, 279-280,
July 2002
© 2002 UK Environmental Mutagen Society/Oxford University Press
DISCUSSION FORUM |
Smoking, lung cancers and their TP53 mutations
Male Urological Cancer Research Centre, Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK
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The TP53 suppressor gene possesses several properties that have facilitated its use as a reporter of genotoxic exposure (Biggs et al., 1993
). In particular, it is mutated in a high proportion of many types of human cancer and it sustains a broad spectrum of mutations that can vary in both their position and type. In lung tumours from smokers, the high frequency of G
T transversions (30% compared with 10% in cancers without tobacco aetiology) has been attributed to DNA adducts of polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene, that are present in tobacco smoke (Hainaut and Pfeifer, 2001). Benzo[a]pyrene is activated to form benzo[a]pyrene diol epoxide (BPDE), which reacts with DNA predominantly at the N2-position of guanine, and both in vitro and in
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