Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monoclonal antibody (HS-63) raised in mice against human ejaculated sperm, polyclonal antibodies raised in rabbits against the cognate mouse testicular antigen (MSA-63; or Fab) and polyclonal antibodies raised in the rabbit against recombinant fusion proteins (GST-63) showed acrosomal localization in permeabilized rhesus monkey and human ejaculated sperm. Tail localization of the cognate primate sperm antigen (PSA-63) was also seen with intact MSA-63 antibodies and Fab fragments. The ability of these antibodies to inhibit sperm binding to the zona pellucida was measured with hemizona binding assays (HZAs). HS-63 (1.2 mg/ml) inhibited rhesus monkey sperm binding (mean +/- SEM) to homologous hemizonae (treatment, 15.5 +/- 3.3; control, 58.9 +/- 9.4; P < 0.025), whereas comparable concentrations of protein from nonimmunized mouse preparations were inactive (ascites fluid, 67.6 +/- 43.5; no ascites fluid, 72.0 +/- 44.6). Intact MSA-63 antibodies inhibited (up to 99%) monkey sperm-zona binding in a concentration-dependent manner. Moreover, inhibition in this case by intact MSA-63 antibody was limited to capacitated sperm. Similarly, intact MSA-63 antibodies inhibited (up to 85%) human sperm binding to homologous zonae in an antibody concentration-dependent manner. Fab fragments derived from MSA-63, when present in insemination mixtures (0.5 mg/ml), inhibited (P < 0.01) primate sperm binding to homologous hemizonae (monkey, 9.6 +/- 3; human sperm 9.4 +/- 2) compared with matched hemizona controls (monkey, 117 +/- 29; human, 20.4 +/- 3). Furthermore, rhesus monkey sperm-zona binding was reduced by 84% in the presence of rabbit anti-GST-63 antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional characterization of the primate sperm acrosomal antigen (PSA-63). 853 49

The polymorphic inheritance of human drug-metabolizing enzymes, such as those encoded by the GST and CYP systems, has been implicated in both cancer risk and prognostic. In an effort to increase our understanding of the interaction between potential environmental exposure, lifestyle, and genetic factors in the predisposition and response to radiotherapy of prostate cancer patients, we examined GSTT1, GSTM1, GSTO1, GSTP1 and CYP1A1 genotypes in a Brazilian population. We studied 125 prostate cancer patients and 100 benign prostatic hyperplasia patients paired for ethnic and lifestyle characteristics. Lifetime occupational history, dietary patterns, cigarette-smoking, and other anamnestic data were obtained through interviews. Outcome was evaluated in 42 stage <or= T2a patients presenting a Gleason score <or= 6, PSA <or= 10 ng/ml, treated with radiotherapy and followed up for 12 to 34 months (15 +/- 8 months). None of the studied polymorphisms was found associated to prostate cancer risk either considered separately or in combination, in uni- or multivariate regression logistic analysis. Also, there was no association between genotypes and possible clinical factors of risk or any parameter of tumour aggressiveness at diagnosis or during follow-up. Patients' response to radiotherapy treatment was not associated to any genotype. In conclusion, our data suggest that GST and CYP1A1 genotypes are not associated with the susceptibility to prostate cancer or its outcome in the Brazilian population.
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PMID:Lack of association of GSTT1, GSTM1, GSTO1, GSTP1 and CYP1A1 polymorphisms for susceptibility and outcome in Brazilian prostate cancer patients. 1864 50