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

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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Meta-Analysis of the Relationship between XRCC1-Arg399Gln and Arg280His Polymorphisms and the Risk of Prostate Cancer

Scientific Reports ◽

10.1038/srep09905 ◽

2015 ◽

Vol 5 (1) ◽

Cited By ~ 10

Author(s):

Jie Yan ◽

Xiantao Wang ◽

Hui Tao ◽

Zengfu Deng ◽

Wang Yang ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Meta Analysis ◽

Prostate Cancer Risk ◽

Recessive Model ◽

Dominant Model ◽

Xrcc1 Arg399gln ◽

Increased Risk ◽

Arg399gln Polymorphism ◽

The Relationship

Abstract Prostate cancer is one of the most common noncutaneous malignancies in Western countries. Because there has been a debate regarding the relationship between the XRCC1-Arg399Gln and Arg280His polymorphisms and prostate cancer risk, we therefore performed this meta-analysis. The electronic databases PubMed, EMBASE and Medline were searched prior to October 1, 2014. An odds ratio and 95% confidence interval were used to calculate association. Heterogeneity was tested by both a chi-square test and I2statistic. Funnel plots and Egger’s test were used to assess publication bias. All statistical analyses were performed using STATA 12.0 software. A significant association between the XRCC1-Arg399Gln polymorphism and prostate cancer risk was found under a homozygote model and a recessive model. A significant association between XRCC1-Arg280His and prostate cancer risk was found under a heterozygote model and a dominant model. Overall, the results of this meta-analysis show that the XRCC1-Arg399Gln polymorphism may be associated with an increased risk for prostate cancer under the homozygote model and the recessive model. And XRCC1-Arg280His polymorphism is likely to be related with prostate cancer risk under the heterozygote model and the dominant model. Additional larger well-designed studies are needed to validate our results.

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

European Journal of Human Genetics ◽

10.1038/ejhg.2008.157 ◽

2008 ◽

Vol 17 (2) ◽

pp. 244-249 ◽

Cited By ~ 23

Author(s):

Li-Xin Qiu ◽

Ru-Tian Li ◽

Jian-Bing Zhang ◽

Wen-Zhao Zhong ◽

Jian-Ling Bai ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Meta Analysis ◽

Prostate Cancer Risk ◽

E Cadherin

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Lack of Association Between CYP17 Mspa1 Polymorphism and Prostate Cancer Risk: A Meta-Analysis of 14 494 Cases and 15 971 Controls

Medicina ◽

10.3390/medicina49020009 ◽

2013 ◽

Vol 49 (2) ◽

pp. 9

Author(s):

Guoqi Song ◽

Ling Gu ◽

Fuliang Tian ◽

Qian Bao ◽

Zhipeng Tang ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Web Of Science ◽

Meta Analysis ◽

Prostate Cancer Risk ◽

Genetic Models ◽

Increased Risk ◽

African Populations ◽

Stratified Analysis ◽

Wide Population

Background and Objective. A T-to-C polymorphism that creates a recognition site for the MspA1 restriction enzyme in the 5’ promoter region of CYP17 has been implicated as a risk factor for prostate cancer. To date, many studies have evaluated associations between the CYP17 MspA1 polymorphism and prostate cancer risk; however, the results were controversial. Therefore, the aim of this study was to perform a meta-analysis to investigate the association between the CYP17 MspA1 polymorphism and the risk of prostate cancer. Material and Methods. By searching the Pubmed, Web of Science, ScienceDirect, EBSCO databases, 36 studies including 14 494 cases and 15 971 controls were collected. Odds ratios (ORs) with their 95% confidence intervals (CIs) were used to assess the strength of the association. Results. The overall results showed no significant association between the CYP17 MspA1 polymorphism and the risk of prostate cancer (OR, 1.07; 95% CI, 0.92–1.25 for A2/A2 vs. A1/A1; OR, 1.02; 95% CI, 0.92–1.12 for A1/A2 vs. A1/A1; OR, 1.07; 95% CI, 0.94–1.22 for A2/A2 vs. A1/A2+A1/A1; OR, 1.03; 95% CI, 0.93–1.14 for A1/A2+A2/A2 vs. A1/A1). In the stratified analysis according to ethnicity, no significant associations were observed in Asian, European, and African populations in all genetic models. In the stratified analysis by the source of controls and inpatients were found to have an increased risk of prostate cancer in all genetic models. Conclusions. The meta-analysis suggests that the CYP17 MspA1 polymorphism is unlikely to increase the risk of prostate cancer in a wide population.

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Positive association between circulating 25-hydroxyvitamin D levels and prostate cancer risk: new findings from an updated meta-analysis

Journal of Cancer Research and Clinical Oncology ◽

10.1007/s00432-014-1706-3 ◽

2014 ◽

Vol 140 (9) ◽

pp. 1465-1477 ◽

Cited By ~ 54

Author(s):

Yonghua Xu ◽

Xiaoping Shao ◽

Yacheng Yao ◽

Lijian Xu ◽

Liang Chang ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Meta Analysis ◽

Prostate Cancer Risk ◽

Positive Association ◽

Hydroxyvitamin D ◽

New Findings ◽

25 Hydroxyvitamin D

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PTGS2–899G>C and prostate cancer risk: a population-based nested case–control study (ProtecT) and a systematic review with meta-analysis

Prostate Cancer and Prostatic Diseases ◽

10.1038/pcan.2009.18 ◽

2009 ◽

Vol 12 (3) ◽

pp. 296-300 ◽

Cited By ~ 8

Author(s):

A Murad ◽

S J Lewis ◽

G Davey Smith ◽

S M Collin ◽

L Chen ◽

...

Keyword(s):

Prostate Cancer ◽

Systematic Review ◽

Cancer Risk ◽

Case Control Study ◽

Meta Analysis ◽

Prostate Cancer Risk ◽

Population Based ◽

Case Control ◽

Nested Case Control ◽

Control Study

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Cancer risk in hyperprolactinemia patients: a population-based cohort study

Acta Endocrinologica ◽

10.1530/eje-11-0076 ◽

2011 ◽

Vol 165 (2) ◽

pp. 209-215 ◽

Cited By ~ 49

Author(s):

Katarina Berinder ◽

Olof Akre ◽

Fredrik Granath ◽

Anna-Lena Hulting

Keyword(s):

Prostate Cancer ◽

Cohort Study ◽

Cancer Risk ◽

Proportional Hazards ◽

Malignant Tumors ◽

Prostate Cancer Risk ◽

Population Based ◽

Cox Proportional Hazards ◽

University Hospital ◽

Increased Risk

ObjectiveExperimental evidence indicates that prolactin might play a role in tumorigenesis of several human cancers, but data on cancer risk in hyperprolactinemia patients are sparse. The aim of this study was to investigate cancer risk in hyperprolactinemia patients.DesignA population-based matched cohort study in Sweden.MethodsThe hyperprolactinemia cohort consisted of patients hospitalized for hyperprolactinemia from 1987 to 1995 identified in the National Patient Register (n=585) and a hospital cohort of prolactinoma patients at Karolinska University Hospital (n=384). For each patient, ten matched individuals were identified via the Register of Population. Cancer occurrence was ascertained via the Swedish Cancer Registry. Hazard ratios (HRs) were estimated by Cox proportional hazards regression.ResultsSeventy-three malignant tumors were identified in the hyperprolactinemia patients and 660 tumors in the comparison group (HR 1.31; 95% confidence interval (CI): 1.02–1.68), mainly attributed to an increased risk of upper gastrointestinal cancer in both males and females (HR 3.69; 95% CI: 1.70–8.03) and hematopoietic cancer in females (HR 3.51; 95% CI: 1.06–11.6). Twelve breast cancers occurred in the female patients, corresponding to an HR of 1.09 (95% CI: 0.60–1.99). Prostate cancer risk in hyperprolactinemia men was reduced (HR 0.40; 95% CI: 0.16–0.99).ConclusionsAn increased overall cancer risk was found in hyperprolactinemia patients, but no increased risk of breast cancer in women and a reduced risk of prostate cancer in men. These findings warrant further investigations and to be confirmed in larger studies but may indicate the importance of an active treatment strategy and follow-up of hyperprolactinemia patients.

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Implications for Prostate Cancer of Insulin-Like Growth Factor-I (IGF-I) Genetic Variation and Circulating IGF-I Levels

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2007-0887 ◽

2007 ◽

Vol 92 (12) ◽

pp. 4820-4826 ◽

Cited By ~ 28

Author(s):

Mattias Johansson ◽

James D. McKay ◽

Fredrik Wiklund ◽

Sabina Rinaldi ◽

Martijn Verheus ◽

...

Keyword(s):

Prostate Cancer ◽

Genetic Variation ◽

Cancer Risk ◽

Association Studies ◽

Meta Analysis ◽

Prostate Cancer Risk ◽

Increased Risk ◽

Igf I ◽

Circulating Levels ◽

I Gene

Abstract Background: Elevated levels of circulating IGF-I have consistently been associated with increased prostate cancer risk. We recently found a haplotype in the 3′ region of the IGF-I gene associated with increased risk of prostate cancer, and we hypothesized that the observed association is mediated by circulating IGF-I. Materials and Methods: We analyzed haplotypes and three haplotype-tagging single nucleotide polymorphisms (htSNPs) in the 3′ region of the IGF-I gene in relation to circulating levels IGF-I in 698 control subjects from the CAncer Prostate in Sweden (CAPS) study and 575 cases and controls from the prospective Northern Sweden Health and Disease Cohort (NSHDC) study. We also performed a meta-analysis of these two and four other association studies on genetic variation in the 3′ region of the IGF-I gene in relation to circulating IGF-I levels. Results: The IGF-I haplotype previously associated with prostate cancer risk, labeled “TCC,” was associated with elevated levels of IGF-I in the CAPS study (P = 0.02), but not in the NSHDC study. In contrast, two of the three IGF-I htSNPs tagging this haplotype, rs6220 and rs7136446, were associated with elevated levels of IGF-I in the NSHDC (P = 0.03 and P = 0.04, respectively), but not in the CAPS study. In the meta-analysis, the TCC haplotype and the rs6220 SNP were associated with elevated levels of circulating IGF-I (P = 0.001 and P < 0.0001, respectively). Conclusions: Genetic variation in the 3′ region of the IGF-I gene seems to influence circulating levels of IGF-I. This observation is consistent with the hypothesis that variation in the IGF-I gene plays a role in prostate cancer susceptibility by influencing circulating levels of IGF-I.

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Social Jetlag and Prostate Cancer Incidence in Alberta’s Tomorrow Project: A Prospective Cohort Study

Cancers ◽

10.3390/cancers12123873 ◽

2020 ◽

Vol 12 (12) ◽

pp. 3873

Author(s):

Liang Hu ◽

Andrew Harper ◽

Emily Heer ◽

Jessica McNeil ◽

Chao Cao ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Cancer Incidence ◽

Repeated Measures ◽

Prospective Cohort ◽

Prostate Cancer Risk ◽

Absolute Difference ◽

Prostate Cancer Incidence ◽

Social Jetlag ◽

Increased Risk

We investigated the association of social jetlag (misalignment between the internal clock and socially required timing of activities) and prostate cancer incidence in a prospective cohort in Alberta, Canada. Data were collected from 7455 cancer-free men aged 35–69 years enrolled in Alberta’s Tomorrow Project (ATP) from 2001–2007. In the 2008 survey, participants reported usual bed- and wake-times on weekdays and weekend days. Social jetlag was defined as the absolute difference in waking time between weekday and weekend days, and was categorized into three groups: 0–<1 h (from 0 to anything smaller than 1), 1–<2 h (from 1 to anything smaller than 2), and 2+ h. ATP facilitated data linkage with the Alberta Cancer Registry in June 2018 to determine incident prostate cancer cases (n = 250). Hazard ratios (HR) were estimated using Cox proportional hazards regressions, adjusting for a range of covariates. Median follow-up was 9.57 years, yielding 68,499 person-years. Baseline presence of social jetlag of 1–<2 h (HR = 1.52, 95% CI: 1.10 to 2.01), and 2+ hours (HR = 1.69, 95% CI: 1.15 to 2.46) were associated with increased prostate cancer risk vs. those reporting no social jetlag (p for trend = 0.004). These associations remained after adjusting for sleep duration (p for trend = 0.006). With respect to chronotype, the association between social jetlag and prostate cancer risk remained significant in men with early chronotypes (p for trend = 0.003) but attenuated to null in men with intermediate (p for trend = 0.150) or late chronotype (p for trend = 0.381). Our findings suggest that greater than one hour of habitual social jetlag is associated with an increased risk of prostate cancer. Longitudinal studies with repeated measures of social jetlag and large samples with sufficient advanced prostate cancer cases are needed to confirm these findings.

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