Human GSTP1 ELISA Matched Antibody Pair

Prostate cancer (CaP) is the most common cancer in men and the second leading cause of cancer deaths in males in Australia. Although serum prostate-specific antigen (PSA) has been the most widely used biomarker in CaP detection for decades, PSA screening has limitations such as low specificity and potential association with over diagnosis. Current biomarkers used in the clinic are not useful for the early detection of CaP, or monitoring its progression, and have limited value in predicting response to treatment. Urine is an ideal body fluid for the detection of protein markers of CaP and is emerging as a potential source for biomarker discovery. Gene-based biomarkers in urine such as prostate cancer antigen-3 (PCA3), and genes for transmembrane protease serine-2 (TMPRSS2), and glutathione S-transferase P (GSTP1) have been developed and evaluated in the past decades. Among these biomarkers, urinary PCA3 is the only one approved by the FDA in the USA for clinical use. The study of urine microRNAs (miRNAs) is another burgeoning area for investigating biomarkers to achieve a pre-biopsy prediction of CaP to contribute to early detection. The development of mass spectrometry (MS)-based proteomic techniques has sparked new searches for novel protein markers for many diseases including CaP. Urinary biomarkers for CaP represent a promising alternative or an addition to traditional biomarkers. Future success in biomarker discovery will rely on collaboration between clinics and laboratories. In addition, research efforts need to be moved from biomarker discovery to validation in a large cohort or separate population of patients and translation of these findings to clinical practice. In this review, we discuss urine as a potential source for CaP biomarker discovery, summarise important genetic urine biomarkers in CaP and focus on MS-based proteomic approaches as well as other recent developments in quantitative techniques for CaP urine biomarker discovery.

Background Prostate cancer is the most common cancer in the world, and its etiology involves the interaction of genetic and environmental factors. Interindividual differences observed in the metabolism of xenobiotics may be due to polymorphisms of genes encoding the detoxification enzymes. This genetic variability seems to be associated with differences in susceptibility to certain types of cancers, including prostate cancer. Our study has been made in order to investigate a possible genetic predisposition to prostate cancer in an Algerian population, through the analysis of genetic polymorphisms of three enzymes metabolizing xenobiotics namelycytochrome P450 (CYP) 1A1, glutathione S-transferase mu 1(GSTM1) andGST theta 1 (GSTT1). Methods The current case-control study included 101 prostate cancer patients and 101 healthy controls. Genotyping ofCYP1A1 T3801Cpolymorphisms andGSTM1/GSTT-nullwas made, respectively, by PCR-RFLP and multiplex PCR. Results No significantly positive associations were found for theCYP1A1 T3801C[p = 0.71, OR = 1.23 (0.56-2.72)] andGSTM1-null[p = 0.26, OR = 1.37 (0.76-2.4)] polymorphisms and prostate cancer susceptibility. However, we detect a highly significant association betweenGSTT1-nullgenotype [p = 0.03, OR = 2.03 (1.06-3.99)],GSTM1/GSTT1-double null genotype [p = 0.027, OR = 2.6; CI (1.07-6.5)] and prostate cancer risk. Furthermore, no statistically significant differences between the studied polymorphisms and tumor parameters (the Gleason score and clinical stages of aggressiveness) at diagnosis of PCa. Conclusions The risk of developing prostate cancer in Algeria does not appear to be associated withCYP1A1 T3801Cgenotypes andGSTM1-null, butGSTT1-nullandGSTM1/GSTT1-double null genotypes increased the risk of prostate cancer.