Methyl group metabolism gene polymorphisms and susceptibility to prostatic carcinoma

The MTHFR C677T Polymorphism and Prostate Cancer Risk: New Findings from a Meta-analysis of 7306 Cases and 8062 Controls

“…Nevertheless, two models examining hospitalbased studies indicated that significant reduced prostate cancer risk was related to the homozygote TT when the study of Kimura (Kimura et al, 2000) was omitted and such effect of SNP C677T was also detected in 3 models assessing population-based studies after the exclusion of Johansson's study (Johansson et al, 2007). The most important and interesting finding of the meta-analysis was the inverse results of the association between the two when measurement was conducted in studies from Asia and Europe respectively.…”

“…From hospital-based studies, we found no significant overall relationship between prostate cancer and the polymorphism under 4 models and great heterogeneity between studies; then sensitivity test detected the study of Kimura et al (2000) influenced the pooled OR substantially, and protective effect of homozygote TT against prostate cancer risk was shown to be significant as well as no heterogeneity found in the rest studies when omitting the above one (TT vs. CC: OR = 0.50, 95%CI = [0.35; 0.71], P < 0.001, I 2 = 0.0%; Recessive: OR = 0.52, 95%CI = [0.37; 0.75], P < 0.001, I 2 =10.3%), which is similar to the overall results. No significant relationship was found between SNP C677T and prostate cancer risk from population-based studies or nested casecontrol studies.…”

“…The relatively low incident rate of prostate cancer in Asian population (American Cancer Society, 2011) and small sample sizes in the recent Asian studies could be the very reason why the protective effect of the polymorphism was diluted in overall studies; it is supported by the sensitivity tests which removed three European studies (Kimura et al, 2000;Heijmans et al, 2003;Collin et al, 2009) respectively from overall studies and detected such protective effect again. However, we still doubt whether it is proper to pool all studies together here to evaluate the association between a polymorphism and prostate cancer risk without the consideration of gene background, living habits and baseline metabolism profile of population in studies.…”

“…According to the background of control population, 6 were hospital-based case-control studies (Kimura et al, 2000;Singal et al, 2004;Marchal et al, 2008;Muslumanoglu et al, 2009;Cai et al, 2010;Wu et al, 2010), 5 were population-based studies (Cicek et al, 2004;Johansson et al, 2007;Reljic et al, 2007;Safarinejad et al, 2010;Kucukhuseyin et al, 2011) and the rest 4 were populationbased studies nested in cohort (Heijmans et al, 2003;Van et al, 2006;Stevens et al, 2008;Collin et al, 2009). One study (Cicek et al, 2004) used sibling as control population.…”

“…Two of the 15 studies were conducted in mixed ethnicities (Cicek et al, 2004;Singal et al, 2004) (Cicek: Caucasian/African-American/Latino; Singal: Caucasian/ African-American), two in yellow Asian (Cai et al, 2010;Wu et al, 2010) and the rests in Caucasian (Kimura et al, 2000;Heijmans et al, 2003;Van et al, 2006;Johansson et al, 2007;Reljic et al, 2007;Marchal et al, 2008;Stevens et al, 2008;Collin et al, 2009;Muslumanoglu et al, 2009;Safarinejad et al, 2010;Kucukhuseyin et al, 2011). In terms of the residential region of the participants, the most recent 5 studies were all conducted in Asia (Muslumanoglu et al, 2009;Cai et al, 2010;Safarinejad et al, 2010;Wu et al, 2010;Kucukhuseyin et al, 2011), 3 of the rest 10 were in the USA (Cicek et al, 2004;Singal et al, 2004;Stevens et al, 2008) and 7 in Europe (Kimura et al, 2000;Heijmans et al, 2003;Van et al, 2006;Johansson et al, 2007;Reljic et al, 2007;Marchal et al, 2008;Collin et al, 2009). All studies extracted DNA from blood/serum samples for further test except one (Singal et al, 2004), in which DNA was isolated from the archived paraffin blocks.…”