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Multifocal accumulation of p53 protein in esophageal carcinoma: Evidence for field cancerization
Author(s) -
Tian Defa,
Feng Zumei,
Hanley Nancy M.,
Setzer R. Woodrow,
Mumford Judy L.,
DeMarini David M.
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19981123)78:5<568::aid-ijc7>3.0.co;2-3
Subject(s) - field cancerization , esophageal cancer , carcinoma , carcinogenesis , pathology , biology , dysplasia , population , carcinoma in situ , cancer , gastroenterology , cancer research , medicine , genetics , environmental health
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 squamous‐cell 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. J. Cancer 78:568–575, 1998. © 1998 Wiley‐Liss, Inc. + This article is a US Government work and, as such, is in the public domain in the United States of America.