{"title":"PTGS2基因8473T>C多态性与前列腺癌风险的相关性:一项包含24,716名受试者的荟萃分析","authors":"Xueling Yang, Bo Li, Tongguo Si, Ya Liu, Zhi Guo","doi":"10.1159/000349951","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Prostaglandin endoperoxide synthase 2 (PTGS2) is involved in prostate cancer (PCa) by stimulating cell proliferation, promoting angiogenesis, inhibiting apoptosis, and mediating immune suppression. 8473T>C, located in the 3' UTR of the PTGS2 gene, has been considered to influence PCa risk.</p><p><strong>Methods: </strong>We searched Medline, PubMed, Elsevier, and Web of Science (updated to February 5, 2012) using the following search terms: '8473T>C' or 'rs5275', 'genetic variant' or 'polymorphism', 'prostate cancer', 'cancer', 'PTGS2' or 'COX-2'. Odds ratios with 95% confidence intervals were assessed by using fixed or random effect models. Both funnel plot and Egger's test were used to assess the publication bias.</p><p><strong>Results: </strong>Finally, 5 case control studies were included. Overall, no evidence was observed of a relationship between the 8473T>C and PCa risk in any genetic model. No significant association was found in the studies whose controls conform to the Hardy-Weinberg equilibrium. In the stratified analysis, significant association was detected in other populations (except for Caucasians), which were based on hospitals.</p><p><strong>Conclusion: </strong>The 8473T>C polymorphism may have little association with PCa risk among Caucasians, but might be involved in PCa risk in other ethnicities. Nevertheless, more well-designed studies with a larger sample size including different ethnicities should be conducted.</p>","PeriodicalId":19684,"journal":{"name":"Onkologie","volume":"36 4","pages":"182-6"},"PeriodicalIF":0.3000,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000349951","citationCount":"7","resultStr":"{\"title\":\"Association between the 8473T>C polymorphism of PTGS2 and prostate cancer risk: a metaanalysis including 24,716 subjects.\",\"authors\":\"Xueling Yang, Bo Li, Tongguo Si, Ya Liu, Zhi Guo\",\"doi\":\"10.1159/000349951\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Prostaglandin endoperoxide synthase 2 (PTGS2) is involved in prostate cancer (PCa) by stimulating cell proliferation, promoting angiogenesis, inhibiting apoptosis, and mediating immune suppression. 8473T>C, located in the 3' UTR of the PTGS2 gene, has been considered to influence PCa risk.</p><p><strong>Methods: </strong>We searched Medline, PubMed, Elsevier, and Web of Science (updated to February 5, 2012) using the following search terms: '8473T>C' or 'rs5275', 'genetic variant' or 'polymorphism', 'prostate cancer', 'cancer', 'PTGS2' or 'COX-2'. Odds ratios with 95% confidence intervals were assessed by using fixed or random effect models. Both funnel plot and Egger's test were used to assess the publication bias.</p><p><strong>Results: </strong>Finally, 5 case control studies were included. Overall, no evidence was observed of a relationship between the 8473T>C and PCa risk in any genetic model. No significant association was found in the studies whose controls conform to the Hardy-Weinberg equilibrium. In the stratified analysis, significant association was detected in other populations (except for Caucasians), which were based on hospitals.</p><p><strong>Conclusion: </strong>The 8473T>C polymorphism may have little association with PCa risk among Caucasians, but might be involved in PCa risk in other ethnicities. Nevertheless, more well-designed studies with a larger sample size including different ethnicities should be conducted.</p>\",\"PeriodicalId\":19684,\"journal\":{\"name\":\"Onkologie\",\"volume\":\"36 4\",\"pages\":\"182-6\"},\"PeriodicalIF\":0.3000,\"publicationDate\":\"2013-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000349951\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Onkologie\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000349951\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2013/3/18 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Onkologie","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000349951","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2013/3/18 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 7
摘要
背景:前列腺素内过氧化物合成酶2 (PTGS2)通过刺激细胞增殖、促进血管生成、抑制细胞凋亡和介导免疫抑制参与前列腺癌(PCa)的发生。8473T>C位于PTGS2基因的3' UTR,被认为影响PCa的风险。方法:我们使用以下搜索词检索Medline、PubMed、Elsevier和Web of Science(更新至2012年2月5日):“8473T>C”或“rs5275”、“遗传变异”或“多态性”、“前列腺癌”、“癌症”、“PTGS2”或“COX-2”。使用固定或随机效应模型评估95%置信区间的比值比。采用漏斗图和Egger检验评估发表偏倚。结果:最终纳入5例病例对照研究。总体而言,没有证据表明在任何遗传模型中8473T>C与PCa风险之间存在关系。在对照符合Hardy-Weinberg平衡的研究中没有发现显著的关联。在分层分析中,在其他以医院为基础的人群(白种人除外)中发现了显著的关联。结论:8473T>C多态性与高加索人PCa风险关系不大,但可能与其他种族的PCa风险有关。然而,应该进行更多设计良好、样本量更大、包括不同种族的研究。
Association between the 8473T>C polymorphism of PTGS2 and prostate cancer risk: a metaanalysis including 24,716 subjects.
Background: Prostaglandin endoperoxide synthase 2 (PTGS2) is involved in prostate cancer (PCa) by stimulating cell proliferation, promoting angiogenesis, inhibiting apoptosis, and mediating immune suppression. 8473T>C, located in the 3' UTR of the PTGS2 gene, has been considered to influence PCa risk.
Methods: We searched Medline, PubMed, Elsevier, and Web of Science (updated to February 5, 2012) using the following search terms: '8473T>C' or 'rs5275', 'genetic variant' or 'polymorphism', 'prostate cancer', 'cancer', 'PTGS2' or 'COX-2'. Odds ratios with 95% confidence intervals were assessed by using fixed or random effect models. Both funnel plot and Egger's test were used to assess the publication bias.
Results: Finally, 5 case control studies were included. Overall, no evidence was observed of a relationship between the 8473T>C and PCa risk in any genetic model. No significant association was found in the studies whose controls conform to the Hardy-Weinberg equilibrium. In the stratified analysis, significant association was detected in other populations (except for Caucasians), which were based on hospitals.
Conclusion: The 8473T>C polymorphism may have little association with PCa risk among Caucasians, but might be involved in PCa risk in other ethnicities. Nevertheless, more well-designed studies with a larger sample size including different ethnicities should be conducted.