The aim of this study was to evaluate the association between glutathione-S-transferase p1 (GSTP1) promoter methylation and the incidence of prostate cancer.
For clinical application, the level as well as the concentration of methylation of glutathione-S transferase-P1 (GSTP1) and EGF-containing fibulin-like extracellular matrix protein 1 (EFEMP1), which are known to be closely associated with prostate cancer diagnosis, are electrochemically detected in human urine spiked with these genes.
Overexpression of Glutathione S-transferase P1 Inhibits the Viability and Motility of Prostate Cancer via Targeting MYC and Inactivating the MEK/ERK1/2 Pathways.
The aim of the present study was to investigate the correlation between the expression of DNA (cytosine‑5)‑methyltransferase 1 (DNMT1), glutathione S‑transferase‑P1 (GSTP1) and adenomatous polyposis coli (APC), and the methylation status of GSTP1 and APC in prostate cancer (PCa) and benign prostatic hyperplasia (BPH), and to examine its clinical significance.
Seventy percent of prostate cancer patients lose expression of transforming growth factor-beta type II receptor (TGFBR2) in the stromal compartment (n=77, P-value=0.0001), similar to the rate of glutathione S-transferase P1 (GSTP1) silencing.
Deletions of the glutathione S-transferase genes M1 and T1 (GSTM1 and GSTT1) have been studied as potential risk factors for prostate cancer.Conflicting results have been obtained.
It has been demonstrated that the glutathione S-transferase (GST) superfamily helps remove carcinogens from the body and thus might be associated with prostate cancer risk.
Many studies have investigated the association between glutathione S-transferase T1 (GSTT1) null genotype and the risk of prostate cancer (PCa), but the impact of GSTT1 null genotype on PCa risk in Caucasians is still unclear owing to the inconsistency of such studies.
Glutathione S-transferases (GSTs) enzymes are involved in conjugation of electrophilic compounds to glutathione, and glutathione S-transferase T 1 (GSTT1) and glutathione S-transferase M 1 (GSTM1) polymorphisms have been implicated as risk factors for prostate cancer.
To improve local staging, the aim of this study was to assess the feasibility of quantitative methylation-specific PCR (Q-MSP) for the identification of promoter hypermethylation of the detoxifying glutathione-S-transferase P1 gene (GSTP1) to detect occult prostate cancer (PCa) cells in the prostatic fossa after RP.
Many studies have investigated the association between glutathione S-transferase T 1 (GSTT1) null genotype and risk of prostate cancer, but the impact of GSTT1 null genotype in Asians is still unclear owing to inconsistencies across results.
Glutathione S-transferase P1 (GSTP1) is hypermethylated in >90% of prostate cancer cases making it one of the most common genome alterations in prostate cancer.
The purpose of this study was to conduct a meta-analysis of the sensitivity and specificity for prostate cancer detection of glutathione-s-transferase-π (GSTP1) methylation in body fluids (plasma, serum, whole blood, urine, ejaculate, and prostatic secretions).
There was no effect modification of glucosinolate intake and cancer risk by GSTA1 (G-52A) or GSTP1 (A313G) genotype, but serum glutathione S-transferase-alpha concentrations were inversely associated with prostate cancer.