ABSTRACT
Following publication of the original article [1], the authors reported a correction in the units in the methods section under "Subjects".
ABSTRACT
<p><b>OBJECTIVES</b>Glutathione S-transferase (GST) A1 catalyses the activated heterocyclic aromatic a mine carcinogenN-acetoxy-2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OAc-PhIP). This case-control study was carried out to examine whether the genetic polymorphism of GSTA1 is associated with the risk oforal squamous cell carcinoma among Japanese people in relation to their smoking status.</p><p><b>METHODS</b>In this study, 97 Japanese oral squamous cell carcinoma patients and 457 healthy controls were compared for the frequencies of theGSTA1 genotypes ((*) A:-567T,-69C,-52G,(*) B:-567G,-69T,-52A).</p><p><b>RESULTS</b>The frequencies ofGSTA1 (*)A/(*)B+(*)B/(*) B genotypes were 32.3% in male cancer patients and 11.4% in female cancer patients, compared with 20.1% in the male control group (Odds ratio (OR)=1.86; 95% confidence interval (CI) 0.99-3.46) and 23.1% in the female control group (OR=0.58; 95% CI 0.18-1.81). TheGSTA1 (*)A/(*)B+(*)B/(*) B genotypes were associated with an 86% increased risk of oral squamous cell carcinoma among males, albeit without statistical significance. Also, among male smokers, the frequency ofGSTA1 (*)A/(*)B+(*)B/(*) B genotypes was significantly higher among the oral squamous cell carcinoma patients (33.3%) than among the controls (19.6%). The OR of the male smokers with theGSTA1 (*)A/(*)B+(*)B/(*) B genotypes for oral squamous cell carcinoma was 1.97 (95% CI 1.02-3.79).</p><p><b>CONCLUSIONS</b>We present the first evidence of an association betweenGSTA1 (*) B and oral squamous cell carcinoma among smokers. This study suggests that the GSTA1 polymorphism and tobacco smoke-derived PhIP are associated with oral squamous cell carcinoma susceptibility among male smokers.</p>
ABSTRACT
Objectives: Glutathione S-transferase (GST) A1 catalyses the activated heterocyclic aromatic amine carcinogen N-acetoxy-2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OAc-PhIP). This case-control study was carried out to examine whether the genetic polymorphism of GSTA1 is associated with the risk of oral squamous cell carcinoma among Japanese people in relation to their smoking status. Methods: In this study, 97 Japanese oral squamous cell carcinoma patients and 457 healthy controls were compared for the frequencies of the GSTA1 genotypes (*A: -567T,-69C,-52G, *B: -567G,-69T,-52A). Results: The frequencies of GSTA1 *A/*B+*B/*B genotypes were 32.3% in male cancer patients and 11.4% in female cancer patients, compared with 20.1% in the male control group (Odds ratio (OR)=1.86; 95% confidence interval (CI) 0.99-3.46) and 23.1% in the female control group (OR=0.58; 95% CI 0.18-1.81). The GSTA1 *A/*B+ *B/*B genotypes were associated with an 86% increased risk of oral squamous cell carcinoma among males, albeit without statistical significance. Also, among male smokers, the frequency of GSTA1 *A/*B+*B/*B genotypes was significantly higher among the oral squamous cell carcinoma patients (33.3%) than among the controls (19.6%). The OR of the male smokers with the GSTA1 *A/*B+ *B/*B genotypes for oral squamous cell carcinoma was 1.97 (95% CI 1.02-3.79). Conclusions: We present the first evidence of an association between GSTA1*B and oral squamous cell carcinoma among smokers. This study suggests that the GSTA1 polymorphism and tobacco smoke-derived PhIP are associated with oral squamous cell carcinoma susceptibility among male smokers.
Subject(s)
Carcinoma, Squamous CellABSTRACT
<p><b>OBJECTIVES</b>To elucidate the association between genetic polymorphisms ofCYP2a6 andCYP2E1 and urothelial cancer susceptibility.</p><p><b>METHODS</b>A total of 137 Japanese patients with urothelial cancer and 217 Japanese healthy controls, frequency-matched for age and gender, were selected. The polymorphisms ofCYP2A6 andCYP2E1 were analyzed by PCR-RFLP, and cigarette smoking histories were obtained through interviews</p><p><b>RESULTS</b>The frequency ofCYP2A6 homozygote deletion genotype was 2.9% in the patients, compared with 3.2% in the controls (OR=0.84, 95% CI 0.24-2.96). The frequencies ofCYP2E1 C1/c2 andC2/c2 were 27.7% and 4.4% in the patients, compared with 35.5% and 6.0% in the controls (OR=0.68, 95% CI 0.42-1.09, OR=0.67, 95% CI 0.24-1.84, respectively). No statistically significant differences were observed when theCYP2A6 homozygote deletion genotype and theCYP2E1 genotypes were examined relative to smoking status.</p><p><b>CONCLUSIONS</b>Our data indicate that neither a relationship between genetically impaired nitrosamine metabolism and tobacco-smoking consumption, nor urothelial cancer risk related to theCYP2A6 deletion genotype andCYP2E1 Rsa I genotype was found in Japanese population.</p>
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Objectives: To elucidate the association between genetic polymorphisms of CYP2A6 and CYP2E1 and urothelial cancer susceptibility. Methods: A total of 137 Japanese patients with urothelial cancer and 217 Japanese healthy controls, frequency-matched for age and gender, were selected. The polymorphisms of CYP2A6 and CYP2E1 were analyzed by PCR-RFLP, and cigarette smoking histories were obtained through interviews. Results: The frequency of CYP2A6 homozygote deletion genotype was 2.9% in the patients, compared with 3.2% in the controls (OR=0.84, 95% CI 0.24−2.96). The frequencies of CYP2E1 C1/c2 and C2/c2 were 27.7% and 4.4% in the patients, compared with 35.5% and 6.0% in the controls (OR=0.68, 95% CI 0.42 −1.09, OR=0.67, 95% CI 0.24−1.84, respectively). No statistically significant differences were observed when the CYP2A6 homozygote deletion genotype and the CYP2E1 genotypes were examined relative to smoking status. Conclusions: Our data indicate that neither a relationship between genetically impaired nitrosamine metabolism and tobacco-smoking consumption, nor urothelial cancer risk related to the CYP2A6 deletion genotype and CYP2E1 Rsa I genotype was found in Japanese population.