Abstract
Background and Objectives N-Acetyltransferase (NAT) 2 is an important enzyme involved in the metabolism of different xenobiotics, including potential carcinogens, whose phenotypes were reported to be related to individual susceptibility to colorectal cancer (CRC). However, the results remain conflicting. To assess the relationship between NAT2 phenotypes and CRC risk, we performed this meta-analysis.MethodsA comprehensive literature search was conducted to identify all case-control or cohort studies of NAT2 acetylator status on the susceptibility of CRC by searching of PubMed and EMBASE, up to May 20, 2011. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the association.ResultsA total of over 40,000 subjects from 40 published literatures were identified by searching the databases. No significantly elevated CRC risk in individuals with NAT2 slow acetylators compared with fast acetylators was found when all studies pooled (OR = 0.95, 95% CI: 0.87–1.04, I2 = 52.6%). While three studies contributed to the source of heterogeneity were removed, there was still null result observed (OR = 0.96, 95% CI: 0.90–1.03, P = 0.17 for heterogeneity, I2 = 17.8%). In addition, we failed to detect any associations in the stratified analyses by race, sex, source of controls, smoking status, genotyping methods or tumor localization. No publication bias was observed in this study.ConclusionsThis meta-analysis suggests that the NAT2 phenotypes may not be associated with colorectal cancer development.
Highlights
Colorectal cancer (CRC) is the third most common cancer among men and women in the U.S, and ranks third as a cause of cancer deaths [1]
After information extraction and discussing, 14 studies were further excluded (7 duplications, 4 without sufficient data, 2 on hereditary nonpolyposis colorectal cancer (HNPCC) and 1 review paper), resulting in 40 eligible studies with 13,896 colorectal cancer (CRC) cases and 18,839 controls reporting the association between the NAT2 acetylator phenotypes and CRC risk for this meta-analysis [9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48]
The result still did not suggest any evidence of publication bias (P = 0.89). This meta-analysis based on 40 studies involving over 40,000 subjects indicates that lack of sufficient evidence supporting the notion of NAT2 phenotypes correlating with the risk of colorectal cancer
Summary
Colorectal cancer (CRC) is the third most common cancer among men and women in the U.S, and ranks third as a cause of cancer deaths [1]. The etiology of CRC is complex and multifactorial. Hereditary syndromes, such as familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC), account for less than 10% of all cases [2]. There is considerable evidence in support of an association between tobacco smoke and colorectal cancer [4]. Another well-established risk factor for CRC is red meat and, processed meat [5]. N-Acetyltransferase (NAT) 2 is an important enzyme involved in the metabolism of different xenobiotics, including potential carcinogens, whose phenotypes were reported to be related to individual susceptibility to colorectal cancer (CRC). To assess the relationship between NAT2 phenotypes and CRC risk, we performed this meta-analysis
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