ALLELIC DELETION IN 11P15 IS A COMMON OCCURRENCE IN ESOPHAGEAL AND GASTRIC ADENOCARCINOMA

BACKGROUND. Esophageal adenocarcinoma and gastric adenocarcinoma have distinct epidemiologic characteristics, but they are morphologically i dentical and sometimes clinically indistinguishable. Recent work in mo lecular oncology suggests that cancer types have distinct molecular ge netic profiles that may explain their biologic differences. Gastric ad enocarcinoma has previously been shown to have a relatively high rate of deletion in chromosome 11. To determine whether similar genetic loc i are involved in esophageal adenocarcinoma, we assayed for genetic lo ss in chromosome 11 in samples of these cancers. METHODS, Dissection o f neoplastic and nonneoplastic tissue was performed under direct micro scopic visualization from histologic sections of 15 gastric adenocarci nomas and 15 esophageal adenocarcinomas. After DNA extraction, polymer ase chain amplification products of a series of polymorphic microsatel lite markers on chromosome 11 were analyzed by polyacrylamide gel elec trophoresis. Tumor specific chromosomal deletion was signaled by the l oss of microsatellite alleles. RESULTS. A panel of 3 polymorphic marke rs in 11p15 revealed overall incidences of loss of heterozygosity (LOH ) of 53.3% in esophageal adenocarcinomas and 61.5% in gastric adenocar cinomas. A panel of 3 polymorphic markers in 11q22-23.3 revealed overa ll incidences of LOH of 14.3% in esophageal adenocarcinomas and 31% in gastric adenocarcinomas. Diffuse microsatellite instability, which wa s consistent with a replication error phenotype, was found in 2 of 15 (13.3%) gastric adenocarcinomas but was not deleted in esophageal aden ocarcinomas. CONCLUSIONS. Esophageal and gastric adenocarcinoma have a similar significant incidence of genetic loss in 11p15. This is sugge stive of the presence of a tumor suppressor gene that may be inactivat ed in both tumor types. Cancer 1998;83:232-9. (C) 1998 American Cancer Society.