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Frequent loss of heterozygosity at the retinoblastoma locus in human esophageal cancers. 1991
R F Boynton, and
Y Huang, and
P L Blount, and
B J Reid, and
W H Raskind, and
R C Haggitt, and
C Newkirk, and
J H Resau, and
J Yin, and
T McDaniel, and
S J Meltzer
Department of Medicine, Gastroenterology Division, University of Maryland, Baltimore.
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.
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