Clinicopathologic and molecular analysis of high-grade dysplasia and earlyadenocarcinoma in short- versus long-segment Barrett esophagus

Barrett esophagus, especially dysplastic Barrett mucosa, has been regarded as a preneoplastic lesion for esophageal adenocarcinoma. However, the etiol ogy and pathogenesis of dysplasia and early adenocarcinoma in short- (SSBE) and long- (LSBE) segment Barrett esophagus have not been studied in detail . The aims of this study were to clarify clinicopathologic and genetic diff erences between high-grade dysplasia (HGD) and early adenocarcinoma in SSBE versus LSBE. We analyzed the clinicopathologic features from 47 patients ( 19 SSBE [<3 cm] and 28 LSBE [<greater than or equal to>3 cm]) with esophage ctomy for HGD/T1 adenocarcinoma. Allelic losses on chromosomes 3p (FIHT), 5 q (APC), 9p (p16), and 17p (p53) were compared in 12 HGD and 9 T1 tumors fr om 19 cases of SSBE and in 23 HGD and 15 T1 tumors from 28 cases of LSBE. P atients with SSBE were more likely to be smokers than were patients with LS BE (94.7% v, 57.1%; P =.004). HGD or T1 tumors arising from SSBE were less likely to show adjoining nondysplastic Barrett mucosa than those from LSBE (73.6% v 100%; P =.02). LSBE more frequently showed a circumferential patte rn of Barrett mucosa than did SSBE (96.4% v 47.3%; P =.0002). Chromosomal a llelic losses on 3p, 5q, Sp, and 17p were detected in 19% (4 of 21), 43% (1 5 of 35), 40% (14 of 35), and 48% (16 of 33) of HGD, respectively, and 26% (5 of 19), 35% (8 of 23), 35% (8 of 23), and 57% (13 of 23) of T1 tumor, re spectively. There were no significant differences in allelic loss of 3p, 5q , 9p, or 17p in HGD or T1 tumors from SSBE versus LSBE. These results sugge st that both HGD and early adenocarcinoma in SSBE and LSBE may occur throug h similar genetic alterations, whereas there are some Clinicopathologic dif ferences between SSBE and LSBE.