Abstract
Endometrial cancer is the seventh most common cancer in women worldwide with an age-standardized rate of 8.4 per 100,000 women. Epigenetic alterations such as promoterhypermethylation of TSGs are known to be early events in carcinogenesis. The aim of the presentstudy, we assessed the aberrant promoter hypermethylation pattern of RAR-β in 78 endometrialcancer samples. Methods: DNA was isolated from endometrial carcinoma samples and normaltissues and aberrant promoter hypermethylation was assessed using nested and methylation-specificPCR. The Chi-square test was used for statistical analysis and a p-value<0.05 was considered to bestatistically significant. Results: 40 of the 78 (51.28%) endometrial carcinoma samples showedaberrant hypermethylation of the RAR-β gene. Methylation status in each histological subtype, gradeand stage of the disease was also assessed. Conclusion: Aberrant hypermethylation is an importantearly epigenetic alteration that occurs during tumorigenesis. The Data shown here reports thatpromoter hypermethylation of RAR-β occurs in endometrial carcinoma and therefore could be usedas a potential marker for early diagnosis and prognosis of the disease.
Highlights
Endometrial cancer (EC) is the seventh most common cancer in women worldwide with an agestandardized incidence rate (ASR) of 8.4 per 100,000 women
Six normal endometrial samples were analyzed for retinoic acid receptors (RARs)-β methylation as a control cohort. 40 of the 78 samples analyzed (51.28%) showed methylation of the RAR-β gene
Aberrant hypermethylation of RAR-β has been studied across various cancer types
Summary
Endometrial cancer (EC) is the seventh most common cancer in women worldwide with an agestandardized incidence rate (ASR) of 8.4 per 100,000 women. Aberrant promoter hypermethylation of Tumor suppressor genes (TSGs) is known to be an early event in many cancers including EC. One of the mechanisms of suppressing the expression of RAR-β is by the epigenetic mechanism of promoter hypermethylation where a methyl group is added to deoxycytidine residues in the CpG islands of its promoter. This methylation of all or a few of the cytosine in the promoter region renders the closure of the chromatin structure eventually resulting in transcriptional silencing of the gene [11,12,13]. We have attempted to analyze the methylation pattern of the RAR-β gene in 78 endometrial cancers of patients of the Indian cohort and associated the methylation patterns with various clinicopathological parameters
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