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Frequent Loss of Heterozygosity at the Retinoblastoma Locus in Human Esophageal Cancers¹

Departments of Medicine (Gastroenterology Division) [R. F. B., J. Y., T. M., S. J. M.], Microbiology and Immunology [Y. H.], Pathology [C. N., J. H. R., S. J. M.], Graduate Program in Molecular and Cell Biology [T. M., S. J. M.], and Cancer Center [S. J. M.], University of Maryland and Department of Veterans Affairs Hospital, Baltimore, Maryland 21201; and Gastroenterology Division [P. L. B., B. J. R.], and Departments of Medicine [P. L. B., B. J. R., W. H. R.], and Pathology [R. C. H.], University of Washington, Seattle, Washington 98195

Abnormalities in the retinoblastoma tumor suppressor gene (Rb) have been observed in a large number of human cancers. Loss of heterozygosity is a common mode of allelic inactivation of Rb and other tumor suppressor genes. We investigated DNA from 61 primary human esophageal tumors for loss of heterozygosity at the Rb locus using a polymerase chain reaction-based restriction fragment length polymorphism assay. Of informative cases, we found loss of heterozygosity in 14 of 26 (54%) squamous cell carcinomas and 5 of 14 (36%) adenocarcinomas. These data support the hypothesis that Rb inactivation is involved in the pathogenesis and/or progression of esophageal cancer.

¹ This work was supported by American Cancer Society Grants PDT-419 and PDT-316B, the Lyn P. Meyerhoff Memorial Research Grant from the Crohn's and Colitis Foundation of America, the Frank C. Bressler Research Fund, the University of Maryland Department of Medicine Research Initiative Fund, NIH Grant P01 DK32971, and the Department of Veterans Affairs.

² To whom requests for reprints should be addressed, at University of Maryland Hospital, Department of Medicine/GI, N3W62, 22 South Greene Street, Baltimore, MD 21201.

Received 7/24/91. Accepted 8/29/91.

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