Significant Association of Catechol-O-Methyltransferase Val158Met Polymorphism with Bladder Cancer Instead of Prostate and Kidney Cancer

2016 ◽  
Vol 31 (2) ◽  
pp. 110-117 ◽  
Author(s):  
Yang Chen ◽  
Xiaoxiang Yu ◽  
Tianyu Li ◽  
Haibiao Yan ◽  
Zengnan Mo
Keyword(s):  
Prostate Cancer ◽  
Bladder Cancer ◽  
Cancer Risk ◽  
Kidney Cancer ◽  
Cancer Susceptibility ◽  
Prostate Cancer Risk ◽  
Comt Val158met ◽  
Val158met Polymorphism ◽  
Urological Cancers ◽  
Codominant Model

Background Urological cancers occur worldwide. Many factors, among which the catechol-O-methyltransferase (COMT) Val158Met polymorphism, are said to be associated with the cancer risk. We conducted a meta-analysis to investigate the association between urological cancer susceptibility and COMT Val158Met in different genetic models. Methods This study was based on material obtained from the PubMed, HuGENet and Embase databases. Four models including dominant (AA + AG vs. GG), recessive (AA vs. AG + GG), codominant (AA vs. AG, AA vs. GG) and per-allele analysis (A vs. G) were applied. Odds ratios (OR) and the corresponding 95% confidence intervals (CI) were used to evaluate the power of the associations. Results Fourteen eligible studies comprising 3,285 cases and 3,594 controls were included. Although we could not detect a positive function of the COMT Val158Met polymorphism in urological cancers, the polymorphism might be significantly associated with bladder cancer risk (dominant model [AA + AG vs. GG]: OR = 0.736, 95% CI = 0.586-0.925, I2 = 0.00%; recessive model [AA vs. AG + GG]: OR = 0.822, 95%CI = 0.653-1.035, I2 = 6.30%; codominant model [AA vs. AG]: OR = 0.908, 95% CI = 0.710-1.161, I2 = 0.00%; codominant model [AA vs. GG]: OR = 0.693, 95% CI = 0.524-0.917, I2 = 30.20%; allele analysis [A vs. G]: OR = 0.826, 95%CI = 0.717-0.951, I2 = 30.20%). The same significant associations were not found for kidney cancer and prostate cancer risk in different ethnicities. There also seemed to be no distinct effect of the polymorphism on benign prostatic hyperplasia. Conclusions We suggest that bladder cancer but not prostate cancer and kidney cancer could be significantly associated with the Val158Met polymorphism. Interaction of COMT genetic and related environmental factors for urological cancers should not be ignored in future.

No Association Between COMT Val158Met Polymorphism and Prostate Cancer Risk: A Meta-Analysis

2013 ◽  
Vol 17 (1) ◽  
pp. 78-84 ◽  
Author(s):  
Li-wei Zou ◽  
Xiao-juan Xu ◽  
Ting Liu ◽  
Han-yong Wang ◽  
Wen-jing Fan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Meta Analysis ◽  
Prostate Cancer Risk ◽  
Comt Val158met ◽  
Val158met Polymorphism

scholarly journals “Catechol-O-methyltransferase gene Val158Met polymorphism and prostate cancersusceptibility”

2020 ◽  
Author(s):  
Pradeep Kumar ◽  
Vandana Rai
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Genetic Model ◽  
Meta Analysis ◽  
Prostate Cancer Risk ◽  
Case Control ◽  
Case Control Studies ◽  
Comt Val158met ◽  
Val158met Polymorphism ◽  
Allele Contrast

AbstractProstate cancer is one of the most common and a serious malignancy of males and it is well reported that estrogen plays a pivotal role in prostate carcinogenesis. Catechol-O - methyltransferase (COMT) catalyzes the inactivation of estrogens. Several studies have investigated the association of COMT gene Val158Metpolymorphism with prostate cancer, but results were inconsistent and inconclusive. Hence, to assess this association, we performed a meta-analysis of all published case-control studies. Pubmed, Springer link, Google Scholar, Elsevier and Springer link databases were searched for case-control studies. Odds ratios (ORs) with 95% confidence intervals (CIs) was used as association measure. Statistical analysis was performed with the software program MIX and MetaAnalyst. In the current meta-analysis, 11 case control studies with 3381 prostate cancer cases and 3,276 healthy controls were considered. The results indicated no significant association between COMT Val158Met polymorphism and prostate cancer risk using allele contrast, co-dominant and homozygote models (allele contrast: OR= 0.92; 95% CI 0.85 to 0.98=; p= 0.02; co-dominant: OR=0.81; 95% CI= 0.85 to1.07; p= 0.46; homozygote: OR= 0.81; 95% CI= 0.70 to 0.95, p= 0.008), but showed significant association with dominant and recessive models (dominant: OR 1.18=; 95% CI= 1.03 to1.34; p= 0.01; recessive: OR= 1.54; 95% CI= 1.1 to 2.07; p = 0.003). In subgroup analysis meta-analysis using recessive genetic model showed significant association between COMT Val 158Met polymorphism and prostate cancer risk in both Asian and Caucasian populations. In conclusion, results of present meta-analysis supports that the COMT Val158Met polymorphism is risk factor for prostate cancer.

scholarly journals Prediction of Breast and Prostate Cancer Risks in Male BRCA1 and BRCA2 Mutation Carriers Using Polygenic Risk Scores

2017 ◽  
Vol 35 (20) ◽  
pp. 2240-2250 ◽  
Author(s):  
Julie Lecarpentier ◽  
Valentina Silvestri ◽  
Karoline B. Kuchenbaecker ◽  
Daniel Barrowdale ◽  
Joe Dennis ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Cancer Susceptibility ◽  
Prostate Cancer Risk ◽  
Risk Scores ◽  
Cancer Risks ◽  
Prostate Cancer Susceptibility ◽  
Common Genetic Variants ◽  
Breast And Prostate Cancer ◽  
Male Carriers

Purpose BRCA1/2 mutations increase the risk of breast and prostate cancer in men. Common genetic variants modify cancer risks for female carriers of BRCA1/2 mutations. We investigated—for the first time to our knowledge—associations of common genetic variants with breast and prostate cancer risks for male carriers of BRCA1/ 2 mutations and implications for cancer risk prediction. Materials and Methods We genotyped 1,802 male carriers of BRCA1/2 mutations from the Consortium of Investigators of Modifiers of BRCA1/2 by using the custom Illumina OncoArray. We investigated the combined effects of established breast and prostate cancer susceptibility variants on cancer risks for male carriers of BRCA1/2 mutations by constructing weighted polygenic risk scores (PRSs) using published effect estimates as weights. Results In male carriers of BRCA1/2 mutations, PRS that was based on 88 female breast cancer susceptibility variants was associated with breast cancer risk (odds ratio per standard deviation of PRS, 1.36; 95% CI, 1.19 to 1.56; P = 8.6 × 10−6). Similarly, PRS that was based on 103 prostate cancer susceptibility variants was associated with prostate cancer risk (odds ratio per SD of PRS, 1.56; 95% CI, 1.35 to 1.81; P = 3.2 × 10−9). Large differences in absolute cancer risks were observed at the extremes of the PRS distribution. For example, prostate cancer risk by age 80 years at the 5th and 95th percentiles of the PRS varies from 7% to 26% for carriers of BRCA1 mutations and from 19% to 61% for carriers of BRCA2 mutations, respectively. Conclusion PRSs may provide informative cancer risk stratification for male carriers of BRCA1/2 mutations that might enable these men and their physicians to make informed decisions on the type and timing of breast and prostate cancer risk management.

scholarly journals Polymorphisms of Homologous RecombinationRAD51,RAD51B,XRCC2, andXRCC3Genes and the Risk of Prostate Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Maria Nowacka-Zawisza ◽  
Ewelina Wiśnik ◽  
Andrzej Wasilewski ◽  
Milena Skowrońska ◽  
Ewa Forma ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Repair ◽  
Cancer Risk ◽  
Cancer Susceptibility ◽  
Critical Role ◽  
Prostate Cancer Risk ◽  
Nucleotide Polymorphisms ◽  
Repair Capacity ◽  
Dna Repair Capacity ◽  
Risk Of Cancer

Genetic polymorphisms in DNA repair genes may induce individual variations in DNA repair capacity, which may in turn contribute to the risk of cancer developing. Homologous recombination repair (HRR) plays a critical role in maintaining chromosomal integrity and protecting against carcinogenic factors. The aim of the present study was to evaluate the relationship between prostate cancer risk and the presence of single nucleotide polymorphisms (SNPs) in the genes involved in HRR, that is,RAD51(rs1801320 and rs1801321),RAD51B(rs10483813 and rs3784099),XRCC2(rs3218536), andXRCC3(rs861539). Polymorphisms were analyzed by PCR-RFLP and Real-Time PCR in 101 patients with prostate adenocarcinoma and 216 age- and sex-matched controls. A significant relationship was detected between theRAD51gene rs1801320 polymorphism and increased prostate cancer risk. Our results indicate that theRAD51gene rs1801320 polymorphism may contribute to prostate cancer susceptibility in Poland.

scholarly journals Breast and prostate cancer risk: the interplay of polygenic risk, high-impact monogenic variants, and family history

2021 ◽  
Author(s):  
Emadeldin Hassanin ◽  
Patrick May ◽  
Rana Aldisi ◽  
Isabel Spier ◽  
Andreas J. Forstner ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Family History ◽  
Cancer Risk ◽  
Cumulative Incidence ◽  
Cancer Susceptibility ◽  
Prostate Cancer Risk ◽  
High Impact ◽  
Polygenic Risk ◽  
Cancer Susceptibility Genes ◽  
Breast And Prostate Cancer

Purpose Investigate to which extent polygenic risk scores (PRS), high-impact monogenic variants, and family history affect breast and prostate cancer risk by assessing cancer prevalence and cancer cumulative lifetime incidence. Methods 200,643 individuals from the UK Biobank were stratified as follows: 1. carriers or non-carriers of high impact constitutive, monogenic variants in cancer susceptibility genes, 2. high or non-high PRS (90th percentile threshold), 3. with or without a family history of cancer. Multivariable logistic regression was used to compare the odds ratio (OR) across the different groups while Cox proportional hazards models were used to compute the cumulative incidence through life. Results Breast and prostate cancer cumulative incidence by age 70 is 7% and 5% for non-carriers with non-high PRS and reaches 37% and 32% among carriers of high-impact variants in cancer susceptibility genes with high PRS. The additional presence of family history is associated with a further increase of the risk of developing cancer reaching an OR of 14 and 21 for breast and prostate cancer, respectively. Conclusion High PRS confers a cancer risk comparable to high-impact monogenic variants. Family history, monogenic variants, and PRS contribute additively to breast and prostate cancer risk.

scholarly journals Do BARD1 Mutations Confer an Elevated Risk of Prostate Cancer?

Cancers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 5464
Author(s):  
Klaudia Stempa ◽  
Dominika Wokołorczyk ◽  
Wojciech Kluźniak ◽  
Emilia Rogoża-Janiszewska ◽  
Karolina Malińska ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Cancer Risk ◽  
Cancer Susceptibility ◽  
Susceptibility Gene ◽  
Prostate Cancer Risk ◽  
Breast Cancer Susceptibility ◽  
Elevated Risk ◽  
Breast Cancer Susceptibility Gene ◽  
Gene Panels

The current cancer testing gene panels tend to be comprehensive rather than site-specific. BARD1 is one of the genes commonly included in the multi-cancer testing panels. Mutations in BARD1 confer an increase in the risk for breast cancer, but it is not studied whether or not they predispose to prostate cancer. To establish if BARD1 mutations also predispose to prostate cancer, we screened BARD1 in 390 Polish patients with hereditary prostate cancer. No truncating mutations were identified by sequencing. We also genotyped 5715 men with unselected prostate cancer, and 10,252 controls for three recurrent BARD1 variants, including p.Q564X, p.R658C and p.R659=. Neither variant conferred elevated risk of prostate cancer (ORs between 0.84 and 1.15, p-values between 0.57 and 0.93) nor did they influence prostate cancer characteristics or survival. We conclude that men with a BARD1 mutation are not at elevated prostate cancer risk. It is not justified to inform men about increased prostate cancer risk in case of identification of a BARD1 mutation. However, a female relative of a man with a BARD1 mutation may benefit from this information and be tested for the mutation, because BARD1 is a breast cancer susceptibility gene.

Lack of Association between COMT Val158Met Polymorphism and Prostate Cancer Susceptibility

2013 ◽  
Vol 91 (2) ◽  
pp. 213-219 ◽  
Author(s):  
Hongtuan Zhang ◽  
Zhihong Zhang ◽  
Jingsheng Wu ◽  
Yong Xu ◽  
Ru Cheng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Susceptibility ◽  
Comt Val158met ◽  
Val158met Polymorphism ◽  
Prostate Cancer Susceptibility

scholarly journals Association of 17 prostate cancer susceptibility loci with prostate cancer risk in Chinese men

The Prostate ◽  
2009 ◽  
Vol 70 (4) ◽  
pp. 425-432 ◽  
Author(s):  
Siqun Lilly Zheng ◽  
Ann W. Hsing ◽  
Jielin Sun ◽  
Lisa W. Chu ◽  
Kai Yu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Cancer Susceptibility ◽  
Prostate Cancer Risk ◽  
Susceptibility Loci ◽  
Chinese Men ◽  
Prostate Cancer Susceptibility

scholarly journals A Rare Variant in ERF (rs144812092) Predisposes to Prostate and Bladder Cancers in an Extended Pedigree

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2399
Author(s):  
Lisa Anne Cannon-Albright ◽  
Craig Carl Teerlink ◽  
Jeff Stevens ◽  
Franklin W. Huang ◽  
Csilla Sipeky ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bladder Cancer ◽  
High Risk ◽  
Cancer Risk ◽  
Rare Variant ◽  
Prostate Cancer Risk ◽  
Cancer Predisposition ◽  
Bladder Cancer Risk ◽  
Extended Pedigree ◽  
Independent Population

Pairs of related bladder cancer cases who belong to pedigrees with an excess of bladder cancer were sequenced to identify rare, shared variants as candidate predisposition variants. Candidate variants were tested for association with bladder cancer risk. A validated variant was assayed for segregation to other related cancer cases, and the predicted protein structure of this variant was analyzed. This study of affected bladder cancer relative pairs from high-risk pedigrees identified 152 bladder cancer predisposition candidate variants. One variant in ERF (ETS Repressing Factor) was significantly associated with bladder cancer risk in an independent population, was observed to segregate with bladder and prostate cancer in relatives, and showed evidence for altering the function of the associated protein. This finding of a rare variant in ERF that is strongly associated with bladder and prostate cancer risk in an extended pedigree both validates ERF as a cancer predisposition gene and shows the continuing value of analyzing affected members of high-risk pedigrees to identify and validate rare cancer predisposition variants.

Sign in / Sign up

Export Citation Format

Share Document