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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Biomarkers, Tumor, Colon, Colonic Neoplasms, DNA Methylation, Gene Expression Regulation, Gene Expression Regulation, Neoplastic, Glucuronidase, Humans, Intestinal Mucosa, Neoplasm Invasiveness, Neoplasm Metastasis, Promoter Regions, Genetic, Sequence Analysis, DNA.
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Do normal colon tissue and colon carcinoma show no difference in heparanase promoter methylation? Context: Heparanase, the sole heparan sulfate degrading enzyme, has a role in cellular invasion. Accordingly, a large number of studies have demonstrated an association between heparanase expression and tumor stage and patients' prognosis. In colon carcinoma, heparanase shows increased expression in tumor compared to normal tissue and its expression correlates with the presence of metastasis. One of the regulatory mechanisms of heparanase expression is de-methylation on its promoter. In the present study we evaluated the role of heparanase promoter methylation in colon carcinoma. Analysis of heparanase promoter methylation was done on 32 samples of colon carcinoma as well as 30 samples of normal colonic mucosa. DNA was extracted from FFPE tissue and subjected to bisulfite conversion. The relative fraction of methylated and unmethylated DNA was evaluated using quantitative real-time PCR. The fraction of methylated DNA was 1 ± 3.4% in the colon carcinoma group, and 2.5 ± 3.3% in the normal colon group (P=0.11). Only one case in the normal group and one case in the tumor group showed more than 10% methylation in the heparanase promoter.
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We did not find any significant difference in heparanase promoter methylation between colon carcinoma and normal colonic mucosa, suggesting that heparanase overexpression in colon carcinoma is mediated by other mechanisms. Final Decision: yes