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Journal Article
Meta-Analysis
Association of MGMT promoter methylation with tumorigenesis features in patients with ovarian cancer: A systematic meta-analysis.
Molecular Genetics & Genomic Medicine 2018 January
BACKGROUND: The MGMT is a key tumor suppressor gene and aberrant promoter methylation has been reported in many cancers. However, the relationship between MGMT promoter methylation and ovarian cancer remains controversial. This meta-analysis was first conducted to estimate the clinical significance of MGMT promoter methylation in ovarian carcinoma.
METHODS: Literature search was performed in the PubMed, Embase, EBSCO and Cochrane Library databases. The pooled odds ratio (OR) and their corresponding 95% confidence interval (95% CI) were summarized.
RESULTS: Final 10 studies with 910 ovarian tissue samples were included in this meta-analysis. MGMT promoter methylation was significantly higher in ovarian cancer than in normal ovarian tissues (OR = 4.13, 95% CI = 2.32-7.33, p < .001). The MGMT had a similar methylation status in cancer versus benign lesions and low malignant potential (LMP) samples (OR = 2.01, 95% CI = 0.67-6.04, p = .212; OR = 1.42, 95% CI = 0.46-4.40, p = .543; respectively). MGMT promoter methylation was correlated with pathological types in which it was significantly lower in serous cancer than in nonserous cancer (OR = 0.29, 95% CI = 0.14-0.59, p = .001). The methylation of the MGMT promoter was not associated with clinical stage and tumor grade (OR = 1.46, 95% CI = 0.71-3.02, p = .301; OR = 1.13, 95% CI = 0.51-2.46, p = .767; respectively).
CONCLUSIONS: MGMT promoter methylation may be correlated with the tumorigenesis of ovarian cancer. It was associated with tumor histotypes, but not correlated with clinical stage and tumor grade. More prospective studies with lager sample sizes are necessary in the future.
METHODS: Literature search was performed in the PubMed, Embase, EBSCO and Cochrane Library databases. The pooled odds ratio (OR) and their corresponding 95% confidence interval (95% CI) were summarized.
RESULTS: Final 10 studies with 910 ovarian tissue samples were included in this meta-analysis. MGMT promoter methylation was significantly higher in ovarian cancer than in normal ovarian tissues (OR = 4.13, 95% CI = 2.32-7.33, p < .001). The MGMT had a similar methylation status in cancer versus benign lesions and low malignant potential (LMP) samples (OR = 2.01, 95% CI = 0.67-6.04, p = .212; OR = 1.42, 95% CI = 0.46-4.40, p = .543; respectively). MGMT promoter methylation was correlated with pathological types in which it was significantly lower in serous cancer than in nonserous cancer (OR = 0.29, 95% CI = 0.14-0.59, p = .001). The methylation of the MGMT promoter was not associated with clinical stage and tumor grade (OR = 1.46, 95% CI = 0.71-3.02, p = .301; OR = 1.13, 95% CI = 0.51-2.46, p = .767; respectively).
CONCLUSIONS: MGMT promoter methylation may be correlated with the tumorigenesis of ovarian cancer. It was associated with tumor histotypes, but not correlated with clinical stage and tumor grade. More prospective studies with lager sample sizes are necessary in the future.
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