TY - JOUR
T1 - CYP2A6 gene deletion reduces susceptibility to lung cancer
AU - Miyamoto, Masami
AU - Umetsu, Yuri
AU - Dosaka-Akita, Hirotoshi
AU - Sawamura, Yuichi
AU - Yokota, Jun
AU - Kunitoh, Hideo
AU - Nemoto, Nobuo
AU - Sato, Kunio
AU - Ariyoshi, Noritaka
AU - Kamataki, Tetsuya
N1 - Funding Information:
Part of this study was supported by a Grant-in-Aid from the Ministry of Education, Science, Sports and Culture of Japan, and a grant from the Japan Health Science Foundation. This work was also supported in part by a Grant-in-Aid from the Ministry of Health and Welfare for the 2nd-term Comprehensive 10-Year Strategy for Cancer Control.
PY - 1999/8/11
Y1 - 1999/8/11
N2 - 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.
AB - 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.
KW - CYP2A6
KW - Epidemiology
KW - Gene deletion
KW - Genetic polymorphism
KW - Lung cancer risk
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U2 - 10.1006/bbrc.1999.1089
DO - 10.1006/bbrc.1999.1089
M3 - Article
C2 - 10441482
AN - SCOPUS:0033546744
SN - 0006-291X
VL - 261
SP - 658
EP - 660
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -
