Prostate cancer is the most common solid cancer and genetic factors play important roles in its pathogenesis. is one of the 8 core genes involved in the nucleotide excision repair pathway. The relationship between Asp312Asn, Lys751Gln, and Arg156Arg polymorphisms in and prostate cancer risk is a controversial topic. Therefore, we conducted a meta-analysis to explore the relationship between these 3 polymorphisms and the risk of developing prostate cancer. We searched the electronic literature in PubMed and Google Scholar for all relevant studies (last updated January 1, 2017). The pooled odds ratios and 95% confidence intervals for the associations between the Asp312Asn, Lys751Gln, or Arg156Arg polymorphisms in and prostate cancer risk were calculated. To evaluate the effects of specific study characteristics on the association of these 3 polymorphisms and prostate cancer risk, we performed subgroup analysis if 2 or more studies were available. After an extensive literature review, 7 publications regarding Asp312Asn genotype distribution with 8 case-controls, 9 publications regarding Lys751Gln genotype distribution with 10 case-controls, and 3 publications regarding Arg156Arg genotype distribution with 4 case-controls were selected. The results showed that Asp312Asn (odds ratio = 1.34, 95% confidence interval: 0.96-1.87, = .000), Lys751Gln (odds ratio = 0.98, 95% confidence interval: 0.89-1.08, = .986), and Arg156Arg (odds ratio = 1.05, 95% confidence interval: 0.91-1.22, = .57) polymorphisms do not increase the risk of prostate cancer in the dominant model. Further, in the subgroup analysis by ethnicity, no relationships were observed between Lys751Gln and Arg156Arg polymorphisms and prostate cancer risk. However, stratified analysis by ethnicity revealed that Asp312Asn affects African (odds ratio = 1.57, 95% confidence interval: 1.06-2.33, = .382) and Asian populations (odds ratio = 2.09, 95% confidence interval: 1.39-3.14, = .396) in homozygote comparison. In conclusion, this meta-analysis suggests that there is no general association between the Asp312Asn, Lys751Gln, and Arg156Arg polymorphisms in and prostate cancer susceptibility.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762072PMC
http://dx.doi.org/10.1177/1533034617724678DOI Listing

Publication Analysis

Top Keywords

prostate cancer
36
95% confidence
24
lys751gln arg156arg
20
arg156arg polymorphisms
20
polymorphisms prostate
20
odds ratio
20
confidence interval
20
asp312asn lys751gln
16
cancer risk
16
genotype distribution
12

Similar Publications

For individuals at high risk of developing breast cancer, interventions to mitigate this risk include surgical removal of their breasts and ovaries or five years treatment with the anti-estrogen tamoxifen or aromatase inhibitors. We hypothesized that a silicone based anti-estrogen-eluting implant placed within the breast would provide the risk reduction benefit of hormonal therapy, but without the adverse effects that limit compliance. To this end, we demonstrate that when placed adjacent to mammary tissue in the 7,12-dimethylbenz[a]anthracene-induced rat breast cancer model a fulvestrant-eluting implant delays breast cancer with minimal systemic exposure.

View Article and Find Full Text PDF

Background And Objective: Selection of patients harboring mutations in homologous recombination repair (HRR) genes for treatment with a PARP inhibitor (PARPi) is challenging in metastatic castration-resistant prostate cancer (mCRPC). To gain further insight, we quantitatively assessed the differential efficacy of PARPi therapy among patients with mCRPC and different HRR gene mutations.

Methods: This living meta-analysis (LMA) was conducted using the Living Interactive Evidence synthesis framework.

View Article and Find Full Text PDF

Incidence and Outcomes of Secondary Bladder Cancer Following Radiation Therapy for Prostate Cancer: A Systematic Review and Meta-analysis.

Eur Urol Focus

January 2025

Department of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria; Department of Urology, Semmelweis University, Budapest, Hungary; Institute for Urology and Reproductive Health, Sechenov University, Moscow, Russia; Department of Urology, UT Southwestern Medical Center, Dallas, TX, USA; Department of Urology, Weill Cornell Medical College, New York, NY, USA; Department of Urology, Second Faculty of Medicine, Charles University, Prague, Czechia; Division of Urology, Department of Special Surgery, University of Jordan, Amman, Jordan; Karl Landsteiner Institute of Urology and Andrology, Vienna, Austria; Research Center for Evidence Medicine, Urology Department, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address:

Background And Objective: There is an established association between secondary bladder cancers (SBCs) and radiotherapy (RT) for prostate cancer (PC), which remains a significant concern. Our aim was to update the evidence on SBC incidence across different RT modalities and to compare oncological outcomes for patients diagnosed with SBC to those diagnosed with primary bladder cancer (PBC).

Methods: We searched MEDLINE, Scopus, and Web of Science for studies on SBC following PC.

View Article and Find Full Text PDF

Radiopharmaceuticals targeting prostate-specific membrane antigen (PSMA) have emerged as a sensitive tool for PET imaging of prostate cancer (PCa) recurrence. Yet urinary bladder activity may obscure the visualization of prostate bed recurrence. Among the Food and Drug Administration-approved PSMA radiopharmaceuticals, F-flotufolastat (rhPSMA-7.

View Article and Find Full Text PDF

Discovery of -(1,2,4-Thiadiazol-5-yl)benzo[]oxepine-4-carboxamide Derivatives as Novel Antiresistance Androgen Receptor Antagonists.

J Med Chem

January 2025

State Key Laboratory of Advanced Drug Delivery and Release Systems, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, China.

The ligand-binding pocket of the androgen receptor (AR) is the targeting site of all clinically used AR antagonists. However, various drug-resistant mutations emerged in the pocket. We previously reported a new targeting site at the dimer interface of AR (dimer interface pocket) and identified a novel antagonist M17-B15 that failed in oral administration.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!