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JNCI Journal of the National Cancer Institute 2000 92(10):782-783; doi:10.1093/jnci/92.10.782
© 2000 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 92, No. 10, 782-783, May 17, 2000
© 2000 Oxford University Press

EDITORIALS

Metabolically Activated Carcinogens and Mutations in the p53 Tumor Suppressor Gene in Lung Cancer

Stephen S. Hecht

Correspondence to: Stephen S. Hecht, Ph.D., University of Minnesota Cancer Center, Box 806 Mayo, 420 Delaware St., S.E., Minneapolis, MN 55455 (e-mail: hecht002@tc.umn.edu).

The article by Smith et al. (1) in this issue of the Journal extends the elegant work of this group on mapping reaction sites of polycyclic aromatic hydrocarbon (PAH) diol epoxides and other activated carcinogens in the p53 tumor suppressor gene (also known as TP53) (2–4). Previously, these investigators (4) have shown that diol epoxides of benzo[a]pyrene (B[a]PDE) and benzo[g]chrysene, as well as N-acetoxy-2-acetylaminofluorene and aflatoxin B1 8,9-epoxide, preferentially bind at methylated CpG sequences in the p53 gene. In the present study (1), they mapped the distribution of adducts induced by diol epoxides of five PAH compounds—5-methylchrysene, 6-methylchrysene, chrysene, . . . [Full Text of this Article]

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