<i>E‐cadherin</i> polymorphism −160 C/A and prostate cancer

Hajdinjak, Tine; Toplak, Nataša

doi:10.1002/ijc.11705

Cited by 14 publications

(4 citation statements)

References 7 publications

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“…The test of heterogeneity for simply a comparison of those three combined ethnicity samples suggested a significant heterogeneity among them (Po0.001). Although the genotype distribution in the studies of Jonsson et al and Pookot et al did not follow Hardy -Weinberg equilibrium, 19,21 the corresponding pooled ORs were not materially altered with or without including these two studies. Similarly, no other single study influenced the pooled OR qualitatively as indicated by sensitivity analyses (data not shown).…”

Section: Study Characteristicsmentioning

confidence: 80%

The E-cadherin (CDH1) −160 C/A polymorphism and prostate cancer risk: a meta-analysis

Qiu

Zhang

et al. 2008

Eur J Hum Genet

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Published data on the association between E-cadherin (CDH1) -160 C/A polymorphism and prostate cancer (PCA) risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. A logistic regression approach proposed for molecular association studies was used to estimate a biological model of the gene effect. A total of 11 studies including 2637 cases and 2673 controls were involved in this meta-analysis. Logistic regression analysis indicated that the CDH1 -160 C/A genotypes were associated with PCA risk. The genetic model test indicated that the genetic model was most likely to be dominant (CA+AA vs CC). Overall, meta-analysis indicated that the -160A allele carriers (CA+AA) had a 21% elevated risk of PCA, when compared with the homozygotes (CC) (odds ratio (OR)=1.21; 95% confidence interval (CI): 0.97-1.51; P=0.090, P(heterogeneity)=0.001). In the subgroup analyses by ethnicity, significantly elevated risks were associated with -160 variant genotypes (CA+AA) in both European and Asian populations (OR=1.24; 95% CI: 1.08-1.43; P=0.003, P(heterogeneity)=0.220 and OR=1.54; 95% CI: 1.23-1.93; P<0.001, P(heterogeneity)=0.200). However, no significant associations were found in Africans (OR=0.59; 95% CI: 0.32-1.09; P=0.090, P(heterogeneity)=0.070). Although some modest bias could not be eliminated, this meta-analysis suggests that the CDH1 -160A allele is a low-penetrant risk factor for developing PCA, especially in Europeans and Asians.

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Section: Study Characteristicsmentioning

confidence: 80%

The E-cadherin (CDH1) −160 C/A polymorphism and prostate cancer risk: a meta-analysis

Qiu

Zhang

et al. 2008

Eur J Hum Genet

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“…Controls selected in studies investigating the association between the -160C/A polymorphism and prostate cancer risk could be divided into healthy [30] , [32] , healthy matched [31] , [33] , [35] , [38] , benign prostatic hyperplasia [29] , healthy and benign prostatic hyperplasia [34] , [37] and benign prostatic hyperplasia or others [36] . Subsequent subgroup analysis stratified by controls in data sets of prostate cancer indicated homogeneity in each strata, indicating that the between-study variance in the prostate subgroup resulted from different controls.…”

Section: Resultsmentioning

confidence: 99%

Contribution of the -160C/A Polymorphism in the E-cadherin Promoter to Cancer Risk: A Meta-Analysis of 47 Case-Control Studies

Wang

et al. 2012

PLoS ONE

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BackgroundThe -160C/A polymorphism (rs16260) of E-cadherin, a tumor repressor gene, has been shown to be a tumor susceptibility allele for various types of cancers. Because the significance of this polymorphism to cancer risk has been recognized, there are increasing studies investigating -160C/A in different types of cancers and ethnic populations. However, there is still uncertainty about the level of risk for a variety of cancers.MethodsTo resolve the controversial question raised by these studies as of March 2012 and provide more statistical power for detecting the significance of -160C/A, we performed a meta-analysis of 47 case-control studies in 16 types of cancers (18,194 cases and 20,207 controls). A meta-regression model and subgroup analysis were employed to identify the source of heterogeneity. Publication bias was evaluated, and sensitivity analysis and cumulative evidence assessment were also performed.ResultsUsing fixed- and random-effects models, the -160AA homozygote was more susceptible to urothelial cancer compared with the -160CA heterozygote. Additionally, the -160A allele is an ethnicity-dependent risk factor for prostate and colorectal cancers. Carriers of the -160A allele in Asians and Europeans were more susceptible to prostate cancer, whereas their North American counterparts seemed tolerant. The -160AA homozygote plays a protective role for Europeans who develop colorectal cancer. The stability of these observations was confirmed by a one-way sensitivity analysis. However, the cumulative evidence for all cancer types was considered ‘weak’ using the Venice guidelines.ConclusionsA meta-analysis indicated that the -160A allele of E-cadherin provides a higher risk for the development of prostate and urothelial cancers and a protective role for colorectal cancer in an ethnicity-dependent manner.

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“…Eight studies focused on the association between the ÿ160A allele and prostate cancer, with 2,633 patients and 2,634 controls (8,(45)(46)(47)(48)(49)(50)(51). Overall meta-analysis showed FIGURE 1.…”

Section: Prostate Cancermentioning

confidence: 99%

The E-cadherin Gene Polymorphism 160C->A and Cancer Risk: A HuGE Review and Meta-Analysis of 26 Case-Control Studies

Wang¹,

Lu²,

Zhang³

et al. 2007

American Journal of Epidemiology

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A single nucleotide polymorphism, - 160C-->A, has been identified in the promoter region of the E-cadherin gene and has been shown to alter its transcriptional activity. To assess susceptibility of -160A allele carriers to seven types of cancers, the authors conducted a comprehensive meta-analysis, up to November 2006, of 26 case-control studies comprising 7,042 cases and 7,011 controls. Pooled odds ratios and 95% confidence intervals were calculated by using the random-effects model. Publication bias, subgroup, and sensitivity analyses were also performed, which showed that -160A allele carriers, compared with noncarriers, had about a 17-19% increased risk of several invasive/metastatic tumors. Analyses of various types of cancers revealed that, in Europeans, the -160AA homozygote was associated with an increased risk of urothelial cancer, carriers of -160A were at increased risk of lung and prostate cancers, and carriers of -160A with gastric cancer were found to suffer a significantly increased risk, whereas their Asian counterparts seemed to be tolerant. No evidence was found that the -160A allele predisposed its carriers to breast, colorectal, or esophageal cancers. These findings indicate that -160A of the E-cadherin gene is emerging as a low-penetrance tumor susceptibility allele for the development of gastric, lung, prostate, and urothelial cancers.

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E‐cadherin polymorphism −160 C/A and prostate cancer

Cited by 14 publications

References 7 publications

The E-cadherin (CDH1) −160 C/A polymorphism and prostate cancer risk: a meta-analysis

The E-cadherin (CDH1) −160 C/A polymorphism and prostate cancer risk: a meta-analysis

Contribution of the -160C/A Polymorphism in the E-cadherin Promoter to Cancer Risk: A Meta-Analysis of 47 Case-Control Studies

The E-cadherin Gene Polymorphism 160C->A and Cancer Risk: A HuGE Review and Meta-Analysis of 26 Case-Control Studies

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