On the excess of G --> T transversions in the p53 gene in lung cancer cell lines. Reply to Pfeifer and Hainaut.
Our recent retrospective analysis of the lung cancer-associated p53 mutation data [Mutat. Res. 508 (2002) 1] showed the possibility of (i) inhibiting action of tobacco smoke on repair of G --> T primary lesions in the non-transcribed strand of the p53 gene and (ii) the origin of new p53 mutations, predominantly G --> T transversions, in lung cancer cell lines apparently unexposed to tobacco smoke. In summary, our arguments suggest that (i) in addition to polycyclic aromatic hydrocarbons (PAH)-DNA adducts there exist other lung cancer-specific, rather than smoke-specific sources of G --> T transversions and (ii) a direct mutagenic action is not the only smoke-associated cause of the prevalence of this class of p53 mutations in lung cancer. In the subsequent critical commentary [Mutat. Res. 526 (2003) 39], Pfeifer and Hainaut suggested our arguments to be "incompatible with available evidence". We would like to address their critique, and appreciate the editors of Mutation Research giving us an opportunity to do so.
Rodin
Sergei N
SN
Rodin
Andrei S
AS
D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics*; D017354:Point Mutation; D012907:Smoking / Q000009:adverse effects; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
D016159:Tumor Suppressor Protein p53