Genetic differences between adenocarcinomas arising in Barrett's esophagus and gastric mucosa.

Abstract

Barrett adenocarcinoma (BA+) and gastric adenocarcinoma comprise a related group of neoplasms that nevertheless have some distinct clinicopathologic characteristics. This study aimed at defining critical molecular abnormalities that may underlie differences between BA+ and gastric adenocarcinomas. We used comparative genomic hybridization for the analyses of 34 xenografts of adenocarcinomas that arose from esophageal or gastric origin. All tumors, except one, exhibited DNA copy number alterations. Losses in 4q and 14q and gains at 2p and 17q were more frequent in proximal (esophageal, gastroesophageal junction [GEJ], and cardia) tumors than in distal (body and antrum) tumors (P <or= 0.050). These changes were significantly higher in BA+ compared with distal tumors (P <or= 0.040). In addition, losses in 5q and gains at 20q were significantly higher in BA+ than in distal cancers (P <or= 0.040). Losses in 5q and 8p and gains at 2q, 6p, 12p, and 20q were significantly more frequent in BA+ tumors (P <or= 0.050) than in GEJ and cardiac tumors without associated Barrett's esophagus. Additionally, losses in 14q, which were common in proximal tumors, were more often seen in BA+ (P = 0.100) than in other proximal tumors. Although these adenocarcinomas share some common genetic alterations, the differences in the DNA copy numbers in BA+ cases suggest that unique genetic alterations may be involved in these cancers' development.