We studied the premalignant nature of achalasia using anti-Ki-67 and anti-p53 monoclonal antibodies immunohistochemically. In this study, four patients with esophageal carcinoma and achalasia were investigated. Three tumors were pT4 (UICC pTNM) and one tumor was pT1. The majority of non-malignant esophageal epithelium showed esophagitis and/or dysplasia histologically. Esophageal epithelial cells in the lesions of esophagitis and/or dysplasia had a higher number of Ki-67-positive cells than normal epithelial cells. p53 protein was expressed in two tumors and it was not expressed in non-malignant epithelium. From these results, we found that esophageal epithelium in achalasia lesions is changed to varying degrees of esophagitis and/or dysplasia by stagnation of intake foods, and these abnormal epithelial cells showed a high proliferative state compared with the normal cells without the p53 gene mutation. We suggest that the distinct proliferative status is a cause of carcinogenesis.

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http://dx.doi.org/10.1046/j.1442-2050.2000.00088.xDOI Listing

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