Increasing cyclooxygenase-2 (cox-2) gene expression in the progression of Barrett's esophagus to adenocarcinoma correlates with that of Bcl-2
✍ Scribed by Daisuke Shimizu; Daniel Vallböhmer; Hidekazu Kuramochi; Kazumi Uchida; Sylke Schneider; Parakrama T. Chandrasoma; Hiroshi Shimada; Tom R. DeMeester; Kathleen D. Danenberg; Jeffrey H. Peters; Steven R DeMeester; Peter V. Danenberg
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- French
- Weight
- 198 KB
- Volume
- 119
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Previous studies from our laboratory and others have suggested that increased expression of cox‐2 is important in the genesis of esophageal adenocarcinoma. In vitro studies suggest that cox‐2 regulates expression of the anti‐apoptotic protein bcl‐2, thus possibly accounting for reduced apoptosis in carcinogenesis. The aim of this study was to investigate the relationship of these 2 genes in the development of Barrett's‐associated adenocarcinoma. Histologic sections from endoscopic biopsies or esophagectomy specimens were classified as non‐dysplastic Barrett's (n = 30), intraepithelial neoplasia (n = 12) and adenocarcinoma (n = 48). The desired tissue was isolated by laser capture microdissection and expression levels of cox‐2 and bcl‐2 were measured by quantitative real‐time PCR (Taqman®). Gene expression levels were compared to samples of the distal esophageal squamous epithelium (n = 55) and reflux‐esophagitis (n = 25), without Barrett's or cancer. Expression of both bcl‐2 and cox‐2 were increased in non‐dysplastic Barrett's (p = 0.0077, p = 0.0037), intraepithelial neoplasia (p = 0.0053, p = 0.0220) and adenocarcinoma (p < 0.0001, p < 0.0001) compared to squamous epithelium or reflux‐esophagitis. Furthermore, there is a significant correlation between these two genes, especially in carcinoma (p < 0.0001). © 2006 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
We have studied the expression of the apoptosis-regulating genes bcl-2, bcl-x, box and APO-I /fas (CD95) in human breast cancer. The expression pattern of these genes in human breast-cancer tissues and breast-cancer-derived cell lines was compared to that seen in normal breast epithelium and breast