ABSTRACT
Background: The intake of red meat and processed meat will increase the risk of colorectal cancer. Heterocyclic amines (HCAs), the intermediate mutagen in the processing of meat food, may be a potential risk factor for meat food to cause cancer. Aims: To investigate the association between HCAs intake and colorectal cancer, thereby providing a basis for prevention of colorectal cancer. Methods: Case-control and cohort studies concerning the association between HCAs intake and colorectal cancer were retrieved from PubMed, Embase, Web of Science, Cochrane Library, CNKI, Wanfang and CQVIP databases. The literature was screened according to the inclusion and exclusion criteria. Meta-analysis was conducted by Stata 12.1 software. Results: A total of 17 studies involving 18 295 colorectal cancer patients were included, of which 14 were case-control studies and 3 were cohort studies. MeIQx intake could increase the risk of colorectal cancer (OR=1.16, 95% CI: 1.01-1.32, P=0.032), DiMeIQx intake (OR=1.20, 95% CI: 1.01-1.43, P=0.045), MeIQx intake (OR=1.24, 95% CI: 1.03-1.50, P=0.023) could increase the risk of colon cancer. No association between PhIP, HCAs and colorectal cancer, colon cancer, or rectal cancer was found. No dose-response relationship between DiMeIQx, MeIQx, PhIP, HCAs and colorectal cancer was found. Conclusions: MeIQx intake may increase the risk of colorectal cancer, DiMeIQx, MeIQx intake may increase the risk of colon cancer, and no dose-response relationship between HCAs intake and colorectal cancer was found.
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>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>