Dataset Information

The mouse double minute 2 309T>G polymorphism and retinoblastoma risk: A meta-analysis.

ABSTRACT:

Purpose

Mouse double minute 2 (MDM2) homolog is a protein that in humans is encoded by the MDM2 gene. It is expressed in retinoblastoma (Rb) cells and acts as a key negative regulator of the p53 tumor suppressor gene. Several studies have investigated the association of Rb with MDM2 309T>G polymorphism, but the results were conflicting. To derive a more precise estimation of the association, we performed a meta-analysis of the relationship between MDM2 309T>G polymorphism with Rb in all published studies.

Methods

Published literature from PubMed and other databases were retrieved. All the reported studies evaluating the association between MDM2 309T>G polymorphism and Rb risk were included. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated using the fixed-effect model. A total of four case-control studies, including 520 cases and 745 controls were included.

Results

This meta-analysis found that MDM2 309T>G polymorphism was significantly associated with Rb risk in the dominant model, TG+GG versus TT (OR = 1.43, 95% CI = 1.11-1.84, P = 0.006).

Conclusion

The present meta-analysis suggested that MDM2 309T>G polymorphism has a significant association with increased Rb risk.

SUBMITTER: Sooraj K

PROVIDER: S-EPMC8081075 | biostudies-literature | 2020 Jul-Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

The mouse double minute 2 309T>G polymorphism and retinoblastoma risk: A meta-analysis.

Sooraj K K Kumar Sunil S Kumar Amit A Bajaj Mandeep S MS Kaur Jasbir J

Saudi journal of ophthalmology : official journal of the Saudi Ophthalmological Society 20200701 3

<h4>Purpose</h4>Mouse double minute 2 (MDM2) homolog is a protein that in humans is encoded by the MDM2 gene. It is expressed in retinoblastoma (Rb) cells and acts as a key negative regulator of the p53 tumor suppressor gene. Several studies have investigated the association of Rb with MDM2 309T>G polymorphism, but the results were conflicting. To derive a more precise estimation of the association, we performed a meta-analysis of the relationship between MDM2 309T>G polymorphism with Rb in all ...[more]

PMID: 34085012

Similar Datasets

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.

Dataset Information

The mouse double minute 2 309T>G polymorphism and retinoblastoma risk: A meta-analysis.

Purpose

Methods

Results

Conclusion

Publications

The mouse double minute 2 309T>G polymorphism and retinoblastoma risk: A meta-analysis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets