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17p Allelic Deletions and p53 Protein Overexpression in Barrett's Adenocarcinoma¹

Departments of Medicine [P. L. B., W. H. R., R. C. H., C. A. S., B. J. R.] and Pathology [R. C. H., P. S. R.], University of Washington, Seattle, Washington 98195; Department of Surgery [S. R.], Ersta Hospital, Stockholm, Sweden; and Department of Pathology [P. J. D.], University of Tennessee Center for the Health Sciences, Memphis, Tennessee 38146

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 population 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.

¹ This work was supported by American Cancer Society Grant PDT 316B, NIH Grant P01 DK32971, Ryan Hill Foundation Fellowship Grant, and Ersta Hospital Research Fund.

² To whom requests for reprints should be addressed, at Division of Gastroenterology RG-24, University of Washington, Seattle, WA 98195.

Received 4/15/91. Accepted 8/ 7/91.

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