P53 EXPRESSION AND PROLIFERATIVE ACTIVITY IN BOWENS-DISEASE WITH OR WITHOUT CHRONIC ARSENIC EXPOSURE

Citation
Tt. Kuo et al., P53 EXPRESSION AND PROLIFERATIVE ACTIVITY IN BOWENS-DISEASE WITH OR WITHOUT CHRONIC ARSENIC EXPOSURE, Human pathology, 28(7), 1997, pp. 786-790
Citations number
22
Categorie Soggetti
Pathology
Journal title
ISSN journal
00468177
Volume
28
Issue
7
Year of publication
1997
Pages
786 - 790
Database
ISI
SICI code
0046-8177(1997)28:7<786:PEAPAI>2.0.ZU;2-S
Abstract
A comparative study of Bowen's disease (ED) with or without chronic ar senic exposure may contribute to understanding arsenic carcinogenesis. We compared the p53 overexpression and proliferative activity of 26 c ases of ED with chronic arsenic exposure (group I) and 22 comparable c ases of ED without chronic arsenic exposure (group II) by immunohistoc hemical method on formalin-fixed, paraffin-embedded tissues with antib odies PAb1801 and MIB-1, respectively. We also included in this study two squamous cell carcinomas that developed from ED in group I and one in group II. Two paired ED lesions in the same individual of one pati ent in group I and of three patients in group II were also studied. Th e significant p53(+) (>10% stained cells) rates were 42.3% (11 of 26) and 9.1% (2 of 22) for groups I and II, respectively, and the differen ce was statistically significant (P=.01). The p53 expression in differ ent lesions of the same individual remained consistently the same. Squ amous cell carcinomas that developed in 2 cases of p53(+) ED in group I were also positive, but the one in 1 case of p53(-) ED in group II w as negative. No significant statistical difference in proliferative ac tivity was found between group I ED and group II ED (P=.769), nor betw een p53(+) cases (>10% stained cells) and p53(-) cases (<10% stained c ells) in group I ED (P=.519). This study showed that significant overe xpression of p53 protein was higher in ED with chronic arsenic exposur e. Therefore, arsenic carcinogenesis of ED might be different from tha t of ED unrelated to arsenic, and alteration of p53 plays a more impor tant role in the pathogenesis of ED with chronic arsenic exposure. Ove rexpression of p53 was not a prerequisite for developing squamous cell carcinoma and was not affected by proliferative activity. HUM PATHOL 28:786-790. Copyright (C) 1997 by W.B. Saunders Company.