Dataset Information

Survivin -31G>C polymorphism and gastrointestinal tract cancer risk: a meta-analysis.

ABSTRACT:

Background

Emerging evidence showed that common functional -31G>C polymorphism (rs9904341 G>C) in the promoter region of the survivin gene is involved in the regulation of survivin expression, thus increasing an individual's susceptibility to gastrointestinal tract (GIT) cancer; but individually published results are inconclusive. The aim of this systematic review and meta-analysis was to derive a more precise estimation of the association between survivin -31G>C polymorphism and GIT cancer risk.

Methods

A literature search of PubMed, Embase, Web of Science and CBM databases was conducted from inception through July 1st, 2012. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association.

Results

Nine case-control studies were included with a total of 2,231 GIT cancer cases and 2,287 healthy controls. The results indicated that survivin -31G>C polymorphism was associated with increased risk of GIT cancer. In the stratified analysis by cancer types, significant associations were observed between survivin -31G>C polymorphism and increased risk of colorectal and gastric cancers. However, the lack of association of survivin -31G>C polymorphism with esophageal cancer risk may be due to a lack of a sufficient number of eligible studies and the influence of different genetic and environmental factors.

Conclusion

Results from the current meta-analysis suggests that survivin -31G>C polymorphism might increase the risk of GIT cancer, especially among gastric and colorectal cancers.

SUBMITTER: Liu Y

PROVIDER: S-EPMC3566135 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Survivin -31G>C polymorphism and gastrointestinal tract cancer risk: a meta-analysis.

Liu Yan Y Li Lin L Qi Haiyan H Gao Yan Y Liu Sha S Xu Chongan C

PloS one 20130206 2

<h4>Background</h4>Emerging evidence showed that common functional -31G>C polymorphism (rs9904341 G>C) in the promoter region of the survivin gene is involved in the regulation of survivin expression, thus increasing an individual's susceptibility to gastrointestinal tract (GIT) cancer; but individually published results are inconclusive. The aim of this systematic review and meta-analysis was to derive a more precise estimation of the association between survivin -31G>C polymorphism and GIT can ...[more]

PMID: 23405077

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Project description:Urinary tract cancer is a common cause of cancer-related death. The etiology and pathogenesis of urinary tract cancer remain unclear, with genetic and epigenetic factors playing an important role. Studies of the polymorphism of murine double minute 2 (MDM2) have shown inconclusive trends in the risk of urinary tract cancer.To clarify this inconsistency, we conducted updated meta-analyses to evaluate the role of MDM2 T309G polymorphism in urinary tract cancer susceptibility.Data sources were Pubmed (1966-May 2015), Chinese biomedicine literature database (1978-May 2015), and hand searching of the reference lists of included studies:(1) research categories case-control study or a nested case-control study; (2) information evaluating the association between the MDM2 SNP309 and urinary tract cancer risk; (3) studies with sufficient data to perform a meta-analysis.It included the use of odds ratios (ORs) to assess the strength of the association, and 95% confidence intervals (CIs) give a sense of the precision of the estimate. We used I for the assessment of between-study heterogeneity, and publication bias was assessed using the funnel plot and the Egger test. Statistical analyses were performed by Review Manage, version 5.0 and Stata 11.0.A total of 18 studies met the eligibility criteria and were included in our analyses. Overall, there was no statistical association between MDM2 SNP309 and prostate cancer risk for the allele contrast, the GG genotype, the recessive genetic model, the dominant genetic model, and prostate cancer risk in all subjects (OR = 0.96, 95% CI 0.87-1.05, P = 0.36; OR = 0.93, 95% CI 0.75-1.15, P = 0.50; OR = 1.00, 95% CI 0.87-1.15, P = 0.99; OR = 0.93, 95% CI 0.80-1.07, P = 0.30), and between MDM2 SNP309 and bladder cancer risk (the allele contrast: OR = 1.06, 95% CI 0.89-1.27, P = 0.50; the GG genotype: OR = 1.12, 95% CI 0.79-1.61, P = 0.52; the dominant genetic model: OR = 1.03, 95% CI 0.83-1.28, P = 0.78; the recessive genetic model: OR = 1.12, 95% CI 0.84-1.49, P = 0.45). However, there was positive association between MDM2 SNP309 and kidney cancer risk for the allele contrast (OR = 1.24, 95% CI 1.05-1.46, P = 0.01), the GG genotype (OR = 1.57, 95% CI 1.11-2.20, P = 0.01), dominant model contrast (OR = 1.30, 95% CI 1.00-1.68, P = 0.05), the recessive genetic model (OR = 1.37, 95% CI 1.02-1.83, P = 0.04).First, only the data of published studies were included in this meta-analysis. Unpublished studies tend to show more negative results; therefore, publication bias may be present. Second, because of the lack of the original data, we did not perform stratification analysis by age, hormone levels, dietary habit, or other variables. This might have caused confounding bias. Third, because the number of studies was relatively small for kidney cancer, the results might not have enough statistical power for us to investigate the association of the polymorphism with kidney cancer susceptibility, and we could not perform subgroup analyses. Finally, there were no studies about Africans in this meta-analysis.In summary, the results of our meta-analysis suggest an increased risk role of the MDM2 SNP T309G in renal cancer. However, there was no association between the MDM2 SNP T309G and prostate cancer risk or between the MDM2 SNP T309G and bladder cancer risk. Moreover, well-designed studies should estimate different ethnicities, degree of malignancy and clinical progression on the association between MDM2 SNP309 and urinary cancer risk in the future.

Project description:BackgroundStimulating food is emerging as an important modifiable factor in the development of gastrointestinal (GI) tract cancers, but the association between chili pepper consumption and the risk of GI cancers is unclear. We aimed to evaluate the direction and magnitude of the association between chili pepper consumption and the risk of GI cancers.MethodsA literature search was performed in PubMed, Embase, and Web of Science databases from inception to 22 December 2021. Observational studies reporting the association between chili pepper consumption and the risk of gastric cancer (GC), esophageal cancer (EC), and/or colorectal cancer (CRC) in adults were eligible for inclusion. Data extraction and quality assessment were conducted independently by two reviewers for the included literature. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a random-effects model. Subgroup analyses were also performed based on the cancer type, study design, region of the study, study quality, and adjustments.ResultsA total of 11,421 studies were screened, and 14 case-control studies were included involving 5009 GI cancers among 11,310 participants. The summary OR showed that high consumption of chili pepper was positively related to the risk of GI cancers (OR = 1.64; 95% CI: 1.00-2.70). A stronger positive relationship was observed between chili pepper consumption and EC risk (OR = 2.71; 95% CI: 1.54-4.75), but there was no statistically significant association between GC and CRC risk. In analyses stratified by geographical location, a positive association was found between chili pepper consumption and the risk of GI cancers in Asian studies (OR = 2.50; 95% CI: 1.23-5.08), African studies (OR = 1.62; 95% CI: 1.04-2.52), and North American studies (OR = 2.61; 95% CI: 1.34-5.08), but an inverse association was seen in South American studies (OR = 0.50; 95% CI: 0.29-0.87) and European studies (OR = 0.30; 95% CI: 0.15-0.61).ConclusionThis meta-analysis suggests that chili pepper is a risk factor for certain GI cancers (e.g., EC). Geographical regions influence the risk of GI cancers, especially in Asian, African, and North American populations, which require more attention during dietary guidance.Systematic review registration[https://www.crd.york.ac.uk/PROSPERO/], identifier [CRD42022320670].

Dataset Information

Survivin -31G>C polymorphism and gastrointestinal tract cancer risk: a meta-analysis.

Background

Methods

Results

Conclusion

Publications

Survivin -31G>C polymorphism and gastrointestinal tract cancer risk: a meta-analysis.

Similar Datasets

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