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  • Title: In situ analysis of p16/INK4 promoter hypermethylation in esophageal carcinoma and gastric carcinoma.
    Author: Zhang F, Wang L, Wu PP, Yan ZW, Zheng L, Yu YY, Jiang XC.
    Journal: Chin J Dig Dis; 2004; 5(4):149-55. PubMed ID: 15612883.
    Abstract:
    OBJECTIVE: Inactivation of the tumor suppressor gene by CpG hypermethylation is a common event in a variety of tumors. The present study was designed to be a comprehensive analysis of p16/INK4 methylation in carcinomas of the upper digestive tract. METHODS: Series of esophageal carcinomas (34 cases) and gastric carcinomas (25 cases) were examined for CpG methylation in p16/INK4 using methylation-specific PCR (MSP). The tissue sections underwent MSP in situ and were then examined microscopically. Immunohistochemical detection of the expression of p16 in the tumor specimens was also performed. RESULTS: Immunohistochemistry detected positive p16 expression in 8 cases of esophageal squamous cell carcinoma and 15 cases of gastric carcinoma. In esophageal carcinoma, hypermethylation of the p16/INK4 promoter region was detected in 5 cases without statistical correlation with its loss of expression, whereas in the gastric carcinomas, p16 expression was positively correlated with the T-classification (r = 0.488, P = 0.01); p16/INK4 methylation was identified in 8 cases. In addition, p16 expression was lower in the methylated samples than in the non-methylated samples (25% vs 76.47%, P = 0.03). Analysis of the MSP-in-situ sections showed that the distribution of methylated cells in esophageal carcinoma differed from that in gastric carcinoma. CONCLUSION: The role of DNA methylation in the silence of p16/INK4 may different between these two types of upper digestive tract tumor.
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