MULTIFOCAL ACCUMULATION OF P53 PROTEIN IN ESOPHAGEAL-CARCINOMA - EVIDENCE FOR FIELD CANCERIZATION

A systematic characterization of the cancerization field of esophageal carcinoma based on p53 protein accumulation has not been reported pre viously. The present report presents such a study based on 50 specimen s of esophageal squamous-cell carcinoma from northern China. To gain i nsight into the etiology of this disease among the 50 subjects, DNA wa s analyzed for a polymorphism of the aldehyde dehydrogenase-2 (ALDH2) gene, which has been associated with increased risk for esophageal can cer among alcohol-consuming patients in Japan, However, the frequency of this polymorphism among our subjects, 30% (15/50), was within publi shed control frequencies for this allele, suggesting that this allele may not play a role in the etiology of esophageal cancer in this north ern Chinese population. Immuno-histochemical staining showed that 66% of the tumors were p53(+). Of 420 pieces near or adjacent to p53(+) tu mors, p53+ cells were present among 64% of basal-cell hyperplasia (BCH ), 70% of dysplasia (DYS) and 88% of carcinoma in situ (CIS). Of 216 p ieces near or adjacent to p53(-) tumors, p53(+) frequencies were 25% o f BCH, 25% of DYS and 0% of CIS. The proportion of BCH cells that were p53+ decreased at increasing distance from the tumor (p = 0.006). The sporadic distribution of p53(+) cells and the distribution and freque ncy of p53(+) precursor lesions support the view that accumulation of p53 protein is multifocal and occurs in precursor lesions in early sta ges of esophageal carcinogenesis. (C) 1998 Wiley-Liss, Inc.(dagger).