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PMID: 1680552 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

17p allelic deletions and p53 protein overexpression in Barrett's adenocarcinoma.

Cancer research ·Vol. 51 ·No. 20 ·1991-10-15 ·Pages 5482-6

Blount PL, Ramel S, Raskind WH, Haggitt RC, Sanchez CA, Dean PJ, Rabinovitch PS, Reid BJ

Abstract

Barrett's esophagus is a condition in which the stratified squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium that predisposes to the development of esophageal adenocarcinoma. Allelic deletions of 17p and alterations of p53 including elevated p53 protein levels have been observed in many different tumors. To investigate the presence of 17p allelic deletions and p53 protein overexpression in Barrett's adenocarcinomas, we have combined the use of restriction fragment length polymorphism analysis, multiparameter flow cytometry, and DNA content cell sorting. The combined use of these methodologies permits the purification of aneuploid tumor cells for restriction fragment length polymorphism analysis of 17p allelic deletions and the evaluation of p53 protein expression by multiparameter flow cytometry in the same aneuploid tumor cell populations. We analyzed 15 aneuploid populations and one tetraploid populations from 13 Barrett's adenocarcinomas for 17p allelic deletions and p53 protein overexpression to determine whether both of these alterations are involved in carcinogenesis in Barrett's esophagus. Twelve of 13 tumors (92%) had 17p allelic deletions, and 8 of 13 tumors (62%) had p53 protein overexpression. Eight of the 12 tumors (67%) with 17p allelic deletions also had p53 protein overexpression. These data indicate that both 17p allelic deletions and p53 protein overexpression are frequently involved in carcinogenesis in Barrett's esophagus.

MeSH Terms
Adenocarcinoma/genetics Alleles Aneuploidy Barrett Esophagus/complications,genetics,metabolism Chromosome Deletion Chromosomes, Human, Pair 17 Esophageal Neoplasms/genetics Humans Polymorphism, Restriction Fragment Length Tumor Suppressor Protein p53/metabolism
Chemicals
Tumor Suppressor Protein p53
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Blount P L
Department of Medicine, University of Washington, Seattle 98195.
Ramel S
Raskind W H
Haggitt R C
Sanchez C A
Dean P J
Rabinovitch P S
Reid B J
Article Info
Journal
Cancer research
Abbr.
Cancer Res
ISSN
0008-5472
Published
1991-10-15
Pages
5482-6
Language
English
Region
United States
NLM ID
2984705R
Subset
IM
Grants
NIDDK NIH HHS · P01 DK32971 · United States
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