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Murine Double Minute 2 SNP T309G Polymorphism and Urinary Tract Cancer Risk

View Article: PubMed Central - PubMed

ABSTRACT

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 I2 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.

No MeSH data available.


Flowchart of meta-analysis.
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Figure 1: Flowchart of meta-analysis.

Mentions: A total of 18 studies 12,14–21,23–31 investigating the polymorphism of MDM2 SNP309 met our inclusion criteria (Figure 1). The characteristics of each study are summarized in Table 1. These studies were published from 2006 to 2015. Eight studies reported the prostate cancer including 4 Asian populations, 3 European populations and 1 USA populations; 7 studies reported the bladder cancer including 3 Asian populations and 4 European populations; and 3 studies reported the renal cancer including 2 Asian populations and 1 European populations, respectively. In all the studies, all controls were free of prostate cancer, bladder cancer, and kidney cancer.


Murine Double Minute 2 SNP T309G Polymorphism and Urinary Tract Cancer Risk
Flowchart of meta-analysis.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998362&req=5

Figure 1: Flowchart of meta-analysis.
Mentions: A total of 18 studies 12,14–21,23–31 investigating the polymorphism of MDM2 SNP309 met our inclusion criteria (Figure 1). The characteristics of each study are summarized in Table 1. These studies were published from 2006 to 2015. Eight studies reported the prostate cancer including 4 Asian populations, 3 European populations and 1 USA populations; 7 studies reported the bladder cancer including 3 Asian populations and 4 European populations; and 3 studies reported the renal cancer including 2 Asian populations and 1 European populations, respectively. In all the studies, all controls were free of prostate cancer, bladder cancer, and kidney cancer.

View Article: PubMed Central - PubMed

ABSTRACT

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 I2 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.

No MeSH data available.