Correction: Association of Polymorphism rs198977 in Human Kallikrein-2 Gene (KLK2) with Susceptibility of Prostate Cancer: A Meta-Analysis
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PROVIDER: S-EPMC3782371 | biostudies-literature | 2013 Jan
REPOSITORIES: biostudies-literature
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Project description:ObjectivesTo assess the association of polymorphism rs198977 in the human kallikrein-2 gene (KLK2) and risk of prostate cancer (PCa).MethodsTwo investigators independently searched the PubMed, Elsevier, EMBASE, Web of Science, Wiley Online Library and Chinese National Knowledge Infrastructure (CNKI). Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) for rs198977 and PCa were calculated in a fixed-effects model (the Mantel-Haenszel method) and a random-effects model (the DerSimonian and Laird method) when appropriate.ResultsSix studies met the inclusion criteria in this meta-analysis, which included 5859 PCa cases and 4867 controls. Overall, rs198977 was associated with the PCa risk (TT+CT vs. CC, pooled OR = 1.163, 95% CI = 1.076-1.258, P-value <0.0001). When stratified by ethnicity, significant association was observed in Caucasian samples under both allele comparison (T vs. C, pooled OR = 1.152, 95% CI = 1.079-1.229, P-value <0.0001) and dominant model (TT+CT vs. CC, pooled OR = 1.197, 95% CI = 1.104-1.297, P-value <0.0001). In the overall analysis, a comparably significant increase in the frequency of allele T for rs198977 was detected between cases and controls in Caucasian.ConclusionThis meta-analysis suggests that rs198977 of KLK2 was associated with susceptibility of PCa in Caucasian and the allele T might increase the risk of PCa in Caucasian.
| S-EPMC3688805 | biostudies-literature
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| S-EPMC4961360 | biostudies-literature
Project description:A number of studies have found that the single nucleotide polymorphisms (SNPs) within the 8q24 region of genome were associated with the susceptibility of prostate cancer. Association between 8q24 SNP variant rs1447295 and higher risk of prostate cancer had been investigated, but those studies were incomplete and the conclusions were obscure.To better elucidate the relationship between rs1447295 polymorphism and the susceptibility of prostate cancer, we performed a more comprehensive meta-analysis about the association between rs1447295 polymorphism and prostate cancer susceptibility by collecting relevant articles published up to November, 2016 and excluding many replicated cohort data existing in previous reports, which made the conclusion more reliant and objective.The results showed that there was a significant prostate cancer risk associated with rs1447295 polymorphism not only in the total groups, but also in American, European and Asian descent subgroups. Meanwhile, a comprehensive analysis about the association between rs1447295 polymorphism and prostate cancer risk were conducted by using different clinical characteristic stratifications including Gleason score, tumor stage and PSA level. The result showed that rs1447295 polymorphism was correlated with different stages of prostate cancer.There are strong association between rs1447295 polymorphism and prostate cancer susceptibility in different ethnic groups and different prostate cancer stage, suggesting that rs1447295 might serve as a reliable biomarker for prostate cancer diagnosis.
| S-EPMC5620154 | biostudies-literature
Project description:ObjectivesAn association of a single nucleotide polymorphism (SNP) of the KLK2 gene (rs198977; c.748C>T; R250W) with risk for developing prostate cancer has been observed. We evaluated the role of R250W SNP for prognosis in prostate cancer.MethodsThe c.748C>T SNP was genotyped from blood DNA of 182 patients after completing initial cancer treatments. For evaluating prognosis of genotype groups, associations were performed with Gleason score (GS) and biochemical recurrence free survival (bRFS) in patients demonstrating PSA-recurrence after initial cancer therapy.ResultsOverall distribution of the CC, CT and TT genotypes for the SNP was 48%, 44% and 8%, respectively. The distribution of high (8-10), moderate (5-7) and low (2-4) GS among the genotype groups was 17%, 74% and 9% for CC group compared to 25%, 74% and 1% for the CT/TT (P=0.04). Median bRFS time for CT/TT group was 36.5 months compared to 44.5 months for the CC group (P=0.16), while genotype groups combined with morphology revealed significantly different bRFS (P=0.004).ConclusionsThis exploratory analysis in prostate cancer patients revealed the W allele of the KLK2 R250W SNP to be less likely associated with low GS morphology. Further studies will be needed to confirm this observation in larger cohorts.
| S-EPMC3982319 | biostudies-literature
Project description:Numerous investigations have addressed the correlation between MMP2-1306C/T polymorphism and prostate cancer (PCa) susceptibility. However, these conclusions were controversial. Thus, we conducted this current meta-analysis based on six studies from PubMed, Embase, Cochrane Library, China Biology Medicine disc (CBM), China National Knowledge Infrastructure (CNKI) up to October 21st, 2016. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to evaluate the strength of the correlations. Additionally, different subgroup analyses and publication bias tests were performed. Eventually, six previous investigations consisted of 1920 cases and 1986 controls were identified and involved in this meta-analysis. Consequently, our evidence indicates a certain association between MMP2-1306C/T polymorphism and PCa risk among overall population (T vs C: OR = 1.12, 95% CI = 1.00-1.24, P = 0.040; TT+CT vs CC: OR = 1.16, 95% CI = 1.02-1.32, P = 0.026; respectively), as well as the subgroups of Asian population (T vs C: OR=1.48, 95% CI=1.13-1.94, P=0.004; TT+CT vs CC: OR = 1.66, 95% CI = 1.21-2.28, P = 0.002; respectively) and PCR-RFLP genotyped method (T vs C: OR = 1.58, 95% CI = 1.19-2.10, P = 0.001; TT+CT vs CC: OR = 1.71, 95% CI = 1.23-2.38, P = 0.001; respectively). However, no association was detected in MMP2-1306C/T polymorphism with Gleason grading or pathological stage of PCa. Our study indicates MMP2-1306 C/T polymorphism might increase PCa risk, particularly for Asian population. However, future studies comprising large cohort size from multicenter are required to confirm our conclusions.
| S-EPMC5546537 | biostudies-other
Project description:BackgroundTo assess the association between polymorphism rs678653 in human Cyclin D1 gene (CCND1) and the risk of cancer.Material/methodsMultiple biomedical databases were systematically searched. Pooled odds ratios (OR) and 95% confidence intervals (95% CIs) were calculated in the appropriate model.ResultsIn total, 17 case-control studies from 14 articles were included. When combing all available data, no significant association of rs678653 with cancer risk was observed under different genetic models. Stratification by ethnicity also indicated that rs678653 was not correlated with cancer risk in Taiwanese or Indian populations. When stratified by cancer type, no significant association was found between polymorphism rs678653 and digestive tract cancer, head and neck cancer, and gynecological cancer risk.ConclusionsOur comprehensive meta-analysis suggests that the polymorphism rs678653 in CCND1 has no association with cancer risk in different population and disease contexts, indicating that CCND1 rs678653 does not serve a significant biological function in predicting cancer risk.
| S-EPMC4798325 | biostudies-literature
Project description:The kallikrein-related peptidase KLK2 has restricted expression in the prostate luminal epithelium, and its protein target is unknown. The present work reports the hydrolytic activities of KLK2 on libraries of fluorescence resonance energy-transfer peptides from which the sequence SYRIF was the most susceptible substrate for KLK2. The sequence SYRIF is present at the extracellular N-terminal segment (58SYRIF63Q) of IL-10R2. KLK2 was fully active at pH 8.0-8.2, found only in prostate inflammatory conditions, and strongly activated by sodium citrate and glycosaminoglycans, the quantities and structures controlled by prostate cells. Bone-marrow-derived macrophages (BMDM) have IL-10R2 expressed on the cell surface, which is significantly reduced after KLK2 treatment, as determined by flow cytometry (FACS analysis). The IL-10 inhibition of the inflammatory response to LPS/IFN-γ in BMDM cells due to decreased nitric oxide, TNF-α, and IL-12 p40 levels is significantly reduced upon treatment of these cells with KLK2. Similar experiments with KLK3 did not show these effects. These observations indicate that KLK2 proteolytic activity plays a role in prostate inflammation and makes KLK2 a promising target for prostatitis treatment.
| S-EPMC11339918 | biostudies-literature
Project description:Introduction: Acute myeloid leukemia (AML) is a heterogeneous myeloid malignancy with abnormal molecular diversity. Tissue kallikrein 2 (KLK2) is a kind of serine protease, and has a close relationship with the occurrence and development of malignant tumors. Single nucleotide polymorphism (SNP) of various genes are associated with susceptibility, treatment and survival of AML. Methods: We investigated the association of KLK2 SNPs rs198977 and rs2664155 with AML. We recruited 284 AML patients and 280 healthy controls from the Han population and genotyping KLK2 SNPs rs198977 and rs2664155 by MassARRAY system. Results: Using clinical data from AML patients and controls, including AML susceptibility, blood count, risk stratification, response to induced chemotherapy and survival, our results showed an increased risk of AML susceptibility with KLK2 rs198977 TT genotype in the recessive model. Regarding white blood cell counts in AML patients, the results showed an increased risk of hyperleukocytosis with the TT genotype of KLK2 rs198977 in a codominant model. Moreover, in the recessive model, AML with KLK2 SNPs rs198977 TT genotype had an increased risk of hyperleukocytosis. No significant correlation was found between KLK2 rs2664155 and AML. Discussion: This study suggests that KLK2 rs198977 may be an important genetic factor in the occurrence of AML and hyperleukocytosis in AML, providing a new perspective for disease progression and new therapeutic targets.
| S-EPMC10427912 | biostudies-literature
Project description:ObjectiveThis meta-analysis aims to explore the association between angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism and susceptibility to prostate cancer (PCa).MethodsWe searched studies related to ACE I/D polymorphism and susceptibility to PCa through PubMed, Web of Science, Embase, Cochrane Library, and Scopus databases from inception to June 1, 2022. Five gene models, including allelic, dominant, recessive, homozygote, and heterozygote models, were analyzed. The pooled odds ratio (OR) was calculated using Stata 15.0 software. Publication bias was judged by the funnel plot and Egger's test, with the robustness of the findings verified by sensitivity analysis.ResultsEight published articles (including ten studies) were identified. The pooled results showed that ACE I/D locus polymorphism was significantly correlated with the risk of PCa under all gene models except for the heterozygous model (D vs. I: OR= 1.58, 95% CI: 1.14-2.21; DD vs. DI+II: OR=1.68, 95% CI: 1.11-2.54; DD+DI vs. II: OR=1.76, 95% CI: 1.11-2.80; DI vs. II: OR= 1.44, 95% CI: 0.99-2.10; DD vs. II: OR= 2.12, 95% CI: 1.15-3.93). Subgroup analysis based on genotype frequencies in the control group meeting Hardy-Weinberg equilibrium showed statistically significant differences in all gene models. The funnel plot and Egger's test indicated no publication bias. The sensitivity analysis verified the robustness of the conclusions obtained in this meta-analysis.ConclusionACE I/D locus polymorphism correlates to PCa risk. Allele D, genotype DD+DI, and DD at the ACE I/D locus increase susceptibility to PCa and can therefore serve as a potential diagnostic and screening molecular marker for PCa patients.
| S-EPMC9635097 | biostudies-literature
Project description:BackgroundGenome-wide association studies have identified rs6465657 polymorphism at chromosome 17q25.3 as a new prostate cancer (PCa) susceptibility locus in people of European descent. However, subsequent replication studies have yielded inconsistent results among different ethnicities. In this study, a comprehensive meta-analysis was conducted to systematically evaluate the relationship between rs6465657 polymorphism and PCa risk.MethodsAll the articles involved were identified from PubMed, EMBASE, Web of Science, EBSCO databases, and Google Scholar before December 2015. The odds ratios (ORs) with corresponding 95% confidence internals (95% CIs) were pooled under the allele model. Fourteen eligible articles with 19 studies were finally included.ResultsIn the overall population, the 17q25.3-rs6465657C allele was found to be significantly associated with increased risk of PCa compared to the T allele (OR =1.097; 95% CI: 1.061-1.134; P<0.001). In the subgroup analysis stratified by ethnicity, significantly increased risk was found in the Caucasian population (OR =1.120; 95% CI: 1.078-1.162; P<0.001), while the difference of OR did not reach the statistical significance in the Asian or African-American population. The analyses of sensitivity indicated the robust stability of the results, and the Begg's and Egger's test indicated that no publication bias existed.ConclusionThe current meta-analysis suggested that the 17q25.3-rs6465657 polymorphism could be associated with PCa susceptibility, especially in the Caucasians, while this association might be different in other ethnicities.
| S-EPMC4966688 | biostudies-literature