A systematic search was performed with the help of various search engines to find out the all the recent studies (2004 to 2015) evaluating the role of GSTM1 and GSTT1 deletion in prostate cancer development.
In summary, this meta-analysis suggested that the null genotype of GSTM1 rather than GSTT1 may be involved in the etiology of prostate cancer in Asian population.
Men with 3, 4 and 5 or more copies of both GSTM1 and GSTT1 genes were at higher risk of prostate cancer (OR: 2.18, 95% CI: 1.21-3.91, OR: 3.24, 95% CI: 1.63-6.46, and OR: 5.77, 95% CI: 1.40-23.84, respectively; P(trend)<0.001).
Thus, the main goal of the present work was to investigate the potential role of single and combined CYP1A1, GSTM1, and GSTT1 genotypes as modifiers of cancer survival in Chilean patients with prostate cancer.
The direction of further research should focus not only on the simple relationship of GSTT1 and prostate cancer but also on gene-environment interaction and distinctions of different GSTs.
Meta-analysis of adjusted ORs also showed a significant association between GSTT1 null genotype and increased risk of prostate cancer (OR= 1.34, 95%CI 1.09-1.64, P = 0.006).
We investigated GSTT1 and GSTM1 genotypes in 429 subjects which included 244 BPH, 51 prostate cancer (PC) patients, and 134 control subjects to find if null genotype in any of the two genes increased the risk of BPH/PC.
In conclusion, GSTM1 and GSTT1 null genotypes are associated with increased risk of prostate cancer in Asians, and GSTM1 and GSTT1 null genotypes are risk factors for the development of prostate cancer.
Despite limitations due to study size, we conclude that the association between HCA intake and PCa risk could be modified by polymorphisms of GSTT1, GSTM1, and MnSOD.
But no association was determined between GSTT1 null genotype (OR = 1.102, 95% CI = 0.9596-1.2655) or GSTP1 A131G polymorphism (OR = 1.0845, 95% CI = 0.96-1.2251) and the PCa risk.
The results obtained demonstrated that simultaneous presence of three potentially risk alleles (GSTM1 null, GSTT1 null and GSTP1 Val) lead to a significant OR increase for PCa.
GSTM1 and GSTT1 null genotype was found to confer 2.5 (OR 2.45; 95% CI 1.56-3.82; P value = 0.00008) and 2.4-fold (OR 2.39; 95% CI 1.36-4.20; P value = 0.002) significant higher risk for prostate cancer.
The hazard ratios (HRs) (95% CIs) for prostate cancer and for death after prostate cancer diagnosis were, respectively, 1.2 (0.8-1.8) and 1.2 (0.6-2.1) for GSTT1*1/0, and 1.8 (1.1-3.0) and 2.2 (1.1-4.4) for GSTT1*0/0 versus GSTT1*1/1.
Presence of GSTM1 null genotype were significantly higher in cancer and BPH group vs. normal individuals (both P values < 0.0001). there was not seen association between GSTT1 null or positive genotype with cancer risk, but analysis of GSTM1 null and GSTT1 positive in combination was statistically associated with Prostate cancer risk (OR = 8.4, 95% CI 1.53-46.73).
Both the GSTM1 and the GSTT1 deletions showed significant inverse associations with prostate cancer [odds ratio (OR): 0.90, 95% confidence interval (CI) 0.83-0.97 and OR 0.88, 95% CI: 0.82-0.96, respectively].
Therefore, we evaluated whether a possible association between glucosinolate intake and prostate cancer risk is modified by polymorphisms in GSTT1, GSTM1, GSTA1, GSTP1, or NOQ1 genes.
We did not observe significantly different crude rates of the GSTM1 and GSTT1 null genotypes in the men diagnosed with prostate cancer and those in the control group.
In conclusion, the major finding of our study suggested that GSTM1 polymorphism conferred an increasing risk of prostate cancer on a wide population basis, however, no relationship was found between GSTT1 and GSTP1 status and the risk of prostate cancer.