Allelic deletion in 11p15 is a common occurrence in esophageal and gastric adenocarcinoma

Abstract

Esophageal adenocarcinoma and gastric adenocarcinoma have distinct epidemiologic characteristics, but they are morphologically identical and sometimes clinically indistinguishable. Recent work in molecular oncology suggests that cancer types have distinct molecular genetic profiles that may explain their biologic differences. Gastric adenocarcinoma has previously been shown to have a relatively high rate of deletion in chromosome 11. To determine whether similar genetic loci are involved in esophageal adenocarcinoma, we assayed for genetic loss in chromosome 11 in samples of these cancers. Dissection of neoplastic and nonneoplastic tissue was performed under direct microscopic visualization from histologic sections of 15 gastric adenocarcinomas and 15 esophageal adenocarcinomas. After DNA extraction, polymerase chain amplification products of a series of polymorphic microsatellite markers on chromosome 11 were analyzed by polyacrylamide gel electrophoresis. Tumor specific chromosomal deletion was signaled by the loss of microsatellite alleles. A panel of 3 polymorphic markers in 11p15 revealed overall incidences of loss of heterozygosity (LOH) of 53.3% in esophageal adenocarcinomas and 61.5% in gastric adenocarcinomas. A panel of 3 polymorphic markers in 11q22-23.3 revealed overall incidences of LOH of 14.3% in esophageal adenocarcinomas and 31% in gastric adenocarcinomas. Diffuse microsatellite instability, which was consistent with a replication error phenotype, was found in 2 of 15 (13.3%) gastric adenocarcinomas but was not deleted in esophageal adenocarcinomas. Esophageal and gastric adenocarcinoma have a similar significant incidence of genetic loss in 11p15. This is suggestive of the presence of a tumor suppressor gene that may be inactivated in both tumor types.