Association of a Genetic Polymorphism of the E-cadherin Gene with Prostate Cancer in a Japanese Population

Kamoto, Toshiyuki; Isogawa, Yoshiaki; Shimizu, Yousuke; Minamiguchi, Sachiko; Kinoshita, Hidefumi; Kakehi, Yoshiyuki; Mitsumori, Kenji; Yamamoto, Shingo; Habuchi, Tomonori; Kato, Takumi; Ogawa, Osamu

doi:10.1093/jjco/hyi040

Cited by 19 publications

(10 citation statements)

References 15 publications

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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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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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“…17 CDH1 C-160A promoter polymorphism was shown to markedly affect CDH1 transcription, thus suppressing CDH1 expression. 18 Several studies have examined the relationship between the CDH1 C-160A polymorphism and cancers of the stomach, [19][20][21] breast, 22 colon, 13,16 bladder [23][24][25] and prostate [26][27][28][29][30][31] with controversial results.…”

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confidence: 99%

The association of cyclin D1 G870A and E‐cadherin C‐160A polymorphisms with the risk of colorectal cancer in a case control study and meta‐analysis

Tan

Nieters

Kropp

et al. 2008

Intl Journal of Cancer

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Cyclin D1 (CCND1) and E-cadherin (CDH1) have been shown to be important genes of the b-catenin/LEF pathway that is involved in colorectal carcinogenesis. However, epidemiological studies on relationship between genetic variants of these two genes and colorectal cancer (CRC) have shown inconsistent results. In a population-based case-control study (498 cases and 600 controls), we assessed the association of CCND1 G870A and CDH1 C-160A polymorphisms with CRC risk. Multivariable logistic regression analysis was used to estimate the association between genotypes, environmental exposures and CRC risk, adjusting for potential confounders. Compared to common homozygotes, the OR for heterozygous and homozygote variant genotype was 1.08 (95% CI, 0.80-1.46) in CCND1 and 0.97 (95% CI, 0.75-1.25) in CDH1. Neither tumor stage nor location showed an association with genetic susceptibility. However, a significant interaction between hormone replacement therapy (HRT) and CCND1 genotypes in CRC risk was found among postmenopausal women (p interaction 5 0.02). The risk reduction associated with HRT was substantial (OR, 0.09; 95% CI, 0.02-0.35) in women who were GG homozygous. A metaanalyses including 11 published studies on CCND1 G870A in addition to our study showed a slightly increased risk of CRC for carriers of the A allele (OR, 1.19; 95% CI, 1.06-1.34); however, there was some indication of publication bias. We conclude that the CCND1 G870A and CDH1 C-160A polymorphisms are not associated with the risk of CRC in the German population. However, the CCND1 G870A polymorphism may modify the protective effect of postmenopausal hormone use on the development of CRC. ' 2008 Wiley-Liss, Inc.Key words: colorectal cancer; cyclin D1; E-cadherin; genetic polymorphism Aberrant activation of Wnt/b-catenin signalling, due to mutations in component enzyme of the pathway, is thought to be an initiating event in colorectal carcinogenesis.1 b-Catenin associates with TCF/LEF (T cell factor/lymphocyte enhancer factor) transcription factors to activate target genes that enhance proliferation and cell survival, and thus impact on the development of colorectal cancer (CRC).2 Therefore, polymorphisms of the genes involved in Wnt/b-catenin signalling pathway are likely to play a role in determining the individual susceptibility to CRC.Cyclin D1 (CCND1) is a key cell cycle regulator from G1 to S phase. The CCND1 gene is a direct target for transactivation by the the b-catenin /LEF-1 pathway through a LEF-1 binding site in the CCND1 promoter.3 A common G870A polymorphism in exon 4 of the CCND1 gene is known to modulate the frequency of alternate splicing and probably reduce transcript levels. 4 A number of studies have linked the CCND1 870A allele to increased cancer risk, but the evidence is not entirely consistent, and some controversy exists regarding the effects on CRC development (Table I). [5][6][7][8][9][10][11][12][13][14][15] E-cadherin (CDH1) is a well-characterized cell-cell adhesion molecule leading to increased cell mobility and possibly i...

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“…One study 10 was eliminated because it did not follow Hardy–Weinberg equilibrium, indicating that these groups might not represent the general population very well. Finally, seven studies 11–17 on CDH1 genotypes and prostate cancer risk including a total of 1294 prostate cancer cases and 1782 controls were identified.…”

Section: Resultsmentioning

confidence: 99%

“…A total of seven publications met the inclusion criteria. 11–17 All of them are case-control studies. Almost all of the cases were histologically confirmed.…”

Section: Resultsmentioning

confidence: 99%

Effect of E-Cadherin (CDH1) −160C/A polymorphism on prostate cancer risk: a meta-analysis

Yang

Wen

et al. 2015

Preprint

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E-Cadherin (CDH1) genetic variations may be involved in invasion and metastasis of various cancers by altering gene transcriptional activity of epithelial cells. However, published studies on the association of CDH1 gene polymorphisms and prostate cancer (PCA)risk remain contradictory, owing to differences in living habits and genetic backgrounds. To derive a more better and comprehensive conclusion, the present meta-analysis was performed. Electronic searches of several databases were conducted for all publications on the association between the CDH1 –160 C/A polymorphism and prostate cancer before Oct 2014. The odds ratio (OR) and its 95% confidence interval (CI) were used for statistical analysis. A total of 7 eligible studies including 1294 cases and 1782 controls were involved in this meta-analysis. Overall, meta-analysis indicated that the −160A allele carriers (AA, CA, AA+CA and A allele) had an increased risk of PCA compared with the homozygotes (CC). In the subgroup analyses by ethnicity, a positive association was found in Asians with A allele, AA, CA, AA+CA genotype and Caucasian descendants with AA genotype, dominant and recessive models. On the contrary, a decreased prostate cancer risk was found in Africans with heterozygous, dominant and allele models. Taken together, this meta-analysis showed that the CDH1 −160A allele might be a risk factor for prostate cancer in Asians and Caucasians. However, this result should be verified by additional population-based studies with large sample sizes.

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Association of a Genetic Polymorphism of the E-cadherin Gene with Prostate Cancer in a Japanese Population

Cited by 19 publications

References 15 publications

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

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

The association of cyclin D1 G870A and E‐cadherin C‐160A polymorphisms with the risk of colorectal cancer in a case control study and meta‐analysis

Effect of E-Cadherin (CDH1) −160C/A polymorphism on prostate cancer risk: a meta-analysis

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