Association between polymorphisms of biotransformation and DNA-repair genes and risk of colorectal cancer in Taiwan

Abstract

The relationship between diet and colorectal cancer has been previously demonstrated and supported with strong epidemiological evidence. The role of genetic polymorphisms has, however, been less well elaborated upon. We conducted a hospital-based case-control study including 727 cases and 736 healthy controls to evaluate the associations of the polymorphic phase-I and -II biotransformations (CYP1A1, CYP1A2, GSTM1, GSTT1, GSTP1, NAT1 and NAT2) and DNA-repair enzymes (XRCC1, XRCC3 and XPD) with the risk of contracting colorectal cancer. We found that men featuring the CYP1A1*2C G/G genotype, the GSTT1 null genotype and XPD 751 with the Gln allele were associated with an elevated risk of colorectal cancer than were men who did not exhibit such genetic features. Multivariate logistic regression analysis revealed that individuals featuring more than two high-risk genotypes increased the colorectal-cancer risk 3.1-fold (OR = 3.1, 95% CI = 1.8-5.2). For women, subjects featuring the CYP1A1*2C G/G genotype and the XRCC3 Thr/Thr genotype faced a 3.1-fold greater risk (95% CI = 1.3-7.0) of colorectal cancer when compared to those featuring the CYP1A1*2C A allele and the XRCC3 Met allele. Taken together, this study suggests that polymorphisms of genes involved in biotransformation and DNA repair could modulate colorectal-cancer risk in Taiwan.

Genotoxic damage in pathology anatomy laboratory workers exposed to formaldehyde

“…The GSTM1 and GSTT1 polymorphisms are the result of the deletion of part of the gene, and this leads to the absence of activity in individuals homozygous for the deletion (null genotype) . The GSTM1 and GSTT1 null genotypes have been associated with increased risk for several cancers including, lung and colorectal cancer (Raimondi et al, 2006;Hosgood et al, 2007;Loft et al, 2007;Yeh et al, 2007). DNA repair is a key human cellular response to DNA-damaging stimuli.…”

GSTM1 and GSTT1 polymorphisms and colorectal cancer risk in Chinese population: a meta-analysis

“…Compared with Economopoulos et al's meta-analysis, our meta-analysis had some differences. Firstly, our meta-analysis included 11 new eligible studies published in Chinese [35-39, 42-44, 47-49] and three new case-control studies published in English [33,34,45], and excluded two studies in Japanese population [52,53] and one study that had overlapping population [20]. At last, we performed this meta-analysis by critically reviewing 19 individual case-control studies (a total of 3,130 CRC cases and 6,423 controls), and the total sample of this new meta-analysis increased to approximately two times (9,553 versus 4,554 [14]).…”

“…According to the exclusion criteria, 13 publications were excluded including nine articles containing overlapping data [20][21][22][23][24][25][26][27][28], two about colorectal adenoma [29,30], one for being case-only study [31], and one for not about GSTT1 or GSTM1 polymorphism [32]. At last, data were available from 19 individual casecontrol studies [33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51] (a total of 3,130 CRC cases and 6,423 controls).…”

Meta-analysis of the relationship between XRCC3 T241M polymorphism and colorectal cancer susceptibility

“…Base on the inclusion criteria, 13 case-control studies with full-text were included in this meta-analysis (Krupa and Blasiak, 2004;Jin et al, 2005;Moreno et al, 2006;Skjelbred et al, 2006;Yeh et al, 2007;Improta et al, 2008;Pardini et al, 2008;Curtin et al, 2009;Canbay et al, 2011;Gil et al, 2012;Zhao et al, 2012;Mucha et al, 2013;Moghtit et al, 2014). The flow chart outlining the criteria used for study selection is shown in Figure 1.…”

“…Among the 13 casecontrol studies, there were 8 studies of Caucasians (Krupa and Blasiak, 2004;Skjelbred et al, 2006;Improta et al, 2008;Pardini et al, 2008;Curtin et al, 2009;Canbay et al, 2011;Gil et al, 2012;Mucha et al, 2013) and 5 studies of Asians (Jin et al, 2005;Moreno et al, 2006;Yeh et al, 2007;Zhao et al, 2012;Moghtit et al, 2014). Nine studies were consistent with HWE for the genotype distribution of the controls (Moreno et al, 2006;Skjelbred et al, 2006;Yeh et al, 2007;Improta et al, 2008;Pardini et al, 2008;Curtin et al, 2009;Gil et al, 2012;Mucha et al, 2013;Moghtit et al, 2014), while 4 were not (Krupa and Blasiak, 2004;Jin et al, 2005;Canbay et al, 2011;Zhao et al, 2012). The baseline characteristics and methodological quality of all studies included are summarized in Table 1.…”