CYP2A6 gene deletion reduces susceptibility to lung cancer

Masami Miyamoto, Yuri Umetsu, Hirotoshi Dosaka-Akita, Yuichi Sawamura, Jun Yokota, Hideo Kunitoh, Nobuo Nemoto, Kunio Sato, Noritaka Ariyoshi, Tetsuya Kamataki

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36 Citations (Scopus)


CYP2A6 is an enzyme with a high ability to activate a nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), to its potent and ultimate carcinogen. In the present study, we investigated the relationship between genetic polymorphism of CYP2A6 and lung cancer risk in a case-control study of Japanese subjects. Genotyping of the CYP2A6 gene in both healthy volunteers and lung cancer patients was conducted. The frequency with which the subjects carried homozygotes of the CYP2A6 gene deletion-type mutation (deletion), which causes lack of the enzyme activity, was lower in the lung cancer patients than in the healthy control subjects. The odds ratio (OR) of the group homozygous for the deletion was significantly lower and calculated to be 0.25 (95% CI; 0.08-0.83) when the OR for the population with homozygotes of the CYP2A6 wild-type gene was defined as 1.00. In the allelic-base analysis, there was also a significant decrease in the OR for the deletion allele. These data suggest that deficient CYP2A6 activity due to genetic polymorphism reduces lung cancer risk.

Original languageEnglish
Pages (from-to)658-660
Number of pages3
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - Aug 11 1999
Externally publishedYes


  • CYP2A6
  • Epidemiology
  • Gene deletion
  • Genetic polymorphism
  • Lung cancer risk

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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