TY - JOUR
T1 - Genetic differences between adenocarcinomas arising in Barrett’s esophagus and gastric mucosa
AU - El-Rifai, Wa’el
AU - Frierson, Henry F.
AU - Moskaluk, Christopher A.
AU - Harper, Jeffrey C.
AU - Petroni, Gina R.
AU - Bissonette, Eric A.
AU - Jones, David R.
AU - Knuutila, Sakari
AU - Powell, Steven M.
N1 - Funding Information:
Supported in part by American Cancer Society grant no. 5-37408.
PY - 2001
Y1 - 2001
N2 - Background & Aims: 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. Methods: We used comparative genomic hybridization for the analyses of 34 xenografts of adenocarcinomas that arose from esophageal or gastric origin. Results: 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 ≤ 0.050). These changes were significantly higher in BA+ compared with distal tumors (P ≤ 0.040). In addition, losses in 5q and gains at 20q were significantly higher in BA+ than in distal cancers (P ≤ 0.040). Losses in 5q and 8p and gains at 2q, 6p, 12p, and 20q were significantly more frequent in BA+ tumors (P ≤ 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. Conclusions: 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.
AB - Background & Aims: 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. Methods: We used comparative genomic hybridization for the analyses of 34 xenografts of adenocarcinomas that arose from esophageal or gastric origin. Results: 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 ≤ 0.050). These changes were significantly higher in BA+ compared with distal tumors (P ≤ 0.040). In addition, losses in 5q and gains at 20q were significantly higher in BA+ than in distal cancers (P ≤ 0.040). Losses in 5q and 8p and gains at 2q, 6p, 12p, and 20q were significantly more frequent in BA+ tumors (P ≤ 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. Conclusions: 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.
UR - http://www.scopus.com/inward/record.url?scp=0034837434&partnerID=8YFLogxK
U2 - 10.1053/gast.2001.27215
DO - 10.1053/gast.2001.27215
M3 - Article
C2 - 11522743
AN - SCOPUS:0034837434
SN - 0016-5085
VL - 121
SP - 592
EP - 598
JO - Gastroenterology
JF - Gastroenterology
IS - 3
ER -