Multifocal accumulation of p53 protein in esophageal carcinoma: Evidence for field cancerization

✍ Scribed by Defa Tian; Zumei Feng; Nancy M. Hanley; R. Woodrow Setzer; Judy L. Mumford; David M. DeMarini

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: French
• Weight: 429 KB
• Volume: 78
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/(sici)1097-0215(19981123)78:5<568::aid-ijc7>3.0.co;2-3

✦ Synopsis

A systematic characterization of the cancerization field of esophageal carcinoma based on p53 protein accumulation has not been reported previously. The present report presents such a study based on 50 specimens of esophageal squamouscell carcinoma from northern China. To gain insight into the etiology of this disease among the 50 subjects, DNA was analyzed for a polymorphism of the aldehyde dehydrogenase-2 (ALDH2) gene, which has been associated with increased risk for esophageal cancer among alcohol-consuming patients in Japan. However, the frequency of this polymorphism among our subjects, 30% (15/50), was within published control frequencies for this allele, suggesting that this allele may not play a role in the etiology of esophageal cancer in this northern Chinese population. Immuno-histochemical staining showed that 66% of the tumors were p53 ؉ . Of 420 pieces near or adjacent to p53 ؉ tumors, p53 ؉ cells were present among 64% of basal-cell hyperplasia (BCH), 70% of dysplasia (DYS) and 88% of carcinoma in situ (CIS). Of 216 pieces near or adjacent to p53 ؊ tumors, p53 ؉ frequencies were 25% of 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 frequency of p53 ؉ precursor lesions support the view that accumulation of p53 protein is multifocal and occurs in precursor lesions in early stages of esophageal carcinogenesis. Int.