<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>24(5)</volume><submitter>Mi Y</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>The association between ribonuclease L (RNASEL) gene polymorphisms and prostate cancer risk has been widely reported, but the results of these studies remained controversial and underpowered. We performed a meta-analysis of 28 studies to evaluate the association between Arg462Gln and Asp541Glu polymorphisms in the RNASEL gene and prostate cancer risk.&lt;h4>Methods&lt;/h4>Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association between RNASEL polymorphisms and prostate cancer risk.&lt;h4>Results&lt;/h4>A significantly increased prostate cancer risk was found for the Arg462Gln polymorphism in Africans (Gln/Gln vs Arg/Arg: OR = 2.50, 95%CI = 1.28-4.87; Gln/Gln vs Gln/Arg + Arg/Arg: OR = 2.54, 95%CI = 1.30-4.95), but not in Europeans and Asians. Additionally, the Asp541Glu polymorphism was associated with increased total prostate cancer risk (Glu-allele vs Asp-allele: OR = 1.04, 95%CI = 1.01-1.07; Glu/Glu vs Asp/Asp: OR = 1.22, 95%CI = 1.03-1.46; Glu/Glu vs Glu/Asp + Asp/Asp: OR = 1.09, 95%CI = 1.02-1.16). In the stratified analysis for the Asp541Glu polymorphism, there was a significantly increased prostate cancer risk in Africans and Europeans, and in hospital-based prostate cancer cases.&lt;h4>Conclusion&lt;/h4>The meta-analysis results showed evidence that RNASEL Arg462Gln and Asp541Glu polymorphisms are associated with prostate cancer risk and could be low-penetrance prostate cancer susceptibility biomarkers.</pubmed_abstract><journal>Journal of biomedical research</journal><pagination>365-73</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3596682</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Arg462Gln and Asp541Glu polymorphisms in ribonuclease L and prostate cancer risk: a meta-analysis.</pubmed_title><pmcid>PMC3596682</pmcid><pubmed_authors>Zhang W</pubmed_authors><pubmed_authors>Feng N</pubmed_authors><pubmed_authors>Mi Y</pubmed_authors><pubmed_authors>Min Z</pubmed_authors><pubmed_authors>Xu B</pubmed_authors><pubmed_authors>Yu Q</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Hua L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Arg462Gln and Asp541Glu polymorphisms in ribonuclease L and prostate cancer risk: a meta-analysis.</name><description>&lt;h4>Objective&lt;/h4>The association between ribonuclease L (RNASEL) gene polymorphisms and prostate cancer risk has been widely reported, but the results of these studies remained controversial and underpowered. We performed a meta-analysis of 28 studies to evaluate the association between Arg462Gln and Asp541Glu polymorphisms in the RNASEL gene and prostate cancer risk.&lt;h4>Methods&lt;/h4>Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association between RNASEL polymorphisms and prostate cancer risk.&lt;h4>Results&lt;/h4>A significantly increased prostate cancer risk was found for the Arg462Gln polymorphism in Africans (Gln/Gln vs Arg/Arg: OR = 2.50, 95%CI = 1.28-4.87; Gln/Gln vs Gln/Arg + Arg/Arg: OR = 2.54, 95%CI = 1.30-4.95), but not in Europeans and Asians. Additionally, the Asp541Glu polymorphism was associated with increased total prostate cancer risk (Glu-allele vs Asp-allele: OR = 1.04, 95%CI = 1.01-1.07; Glu/Glu vs Asp/Asp: OR = 1.22, 95%CI = 1.03-1.46; Glu/Glu vs Glu/Asp + Asp/Asp: OR = 1.09, 95%CI = 1.02-1.16). In the stratified analysis for the Asp541Glu polymorphism, there was a significantly increased prostate cancer risk in Africans and Europeans, and in hospital-based prostate cancer cases.&lt;h4>Conclusion&lt;/h4>The meta-analysis results showed evidence that RNASEL Arg462Gln and Asp541Glu polymorphisms are associated with prostate cancer risk and could be low-penetrance prostate cancer susceptibility biomarkers.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Sep</publication><modification>2024-12-03T16:46:15.093Z</modification><creation>2019-03-27T01:06:02Z</creation></dates><accession>S-EPMC3596682</accession><cross_references><pubmed>23554651</pubmed><doi>10.1016/S1674-8301(10)60049-8</doi></cross_references></HashMap>