Abstract
Abstract Aim: Barrett's esophagus (BE) is a premalignant condition, predisposing to esophageal adenocarcinoma (EAC). However, some EAC arise in columnar lined esophageal mucosa devoid of goblet cells. Therefore, the purpose of this study was to evaluate the biological properties of non-goblet columnar lined esophagus (CLE) and elucidate the relationship between BE and high grade dysplasia of esophagus (HGD). Material and Methods: Endoscopic biopsies from esophagus of 47 patients with columnar metaplasia with goblet cells (BE; n=28), columnar metaplasia with non-goblet cell (CLE; n=10), BE associated high grade dysplasia (HGD; n=9) and cardia with intestinal metaplasia (CIM; n=5) were included in the study. These groups were immunostained for, Villin (intestinal marker), CK7 (columnar epithelium marker), Claudin 3 (epithelial tight-junction marker) and MUC4 (membranous mucin). Statistical analysis between different groups was performed using the paired or unpaired t- test using SPSS v 15.0. A p value <0.05 was considered significant. Results: Patients with BE, CLE and HGD showed positivity for Villin, Claudin 3 and CK7 in 79%, 93%, 54% in BE group; 60%, 100% and 80% in CLE group and 78%, 100% and 34% in HGD group respectively. In metaplastic epithelium (BE and CLE) there was no statistically significant difference in expression of these markers (p>0.05). Patients with CLE without goblet cells showed immunopositive results for these markers, statistically similar to those of HGD group and also revealed significantly higher values compared to those of controls (cardia with intestinal metaplasia). MUC4 was expressed higher in 96% of BE cases as compared to 67% of HGD cases (mean, 81.85±27.74 vs 48.89±45.12). CLE without goblet cells did not express MUC4. Conclusion: Our results indicate that metaplastic columnar lined epithelium without goblet cells suggest biological properties of intestinal differentiation. It also shows that apart from BE, CLE without goblet cells may also have neoplastic potential. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 735. doi:1538-7445.AM2012-735
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