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Publication Detail

Title: Increased expression and secretion of interleukin-6 in patients with Barrett's esophagus.

Authors: Dvorakova, Katerina; Payne, Claire M; Ramsey, Lois; Holubec, Hana; Sampliner, Richard; Dominguez, Jessica; Dvorak, Bohuslav; Bernstein, Harris; Bernstein, Carol; Prasad, Anil; Fass, Ronnie; Cui, Haiyan; Garewal, Harinder

Published In Clin Cancer Res, (2004 Mar 15)

Abstract: Barrett's esophagus (BE) is a common premalignant lesion of the distal part of the esophagus that arises as a consequence of chronic duodenogastroesophageal reflux. Interleukin (IL)-6 is a pleiotropic cytokine that regulates immune defense mechanisms and hematopoiesis. In addition, IL-6 may also be involved in malignant transformation and tumor progression. IL-6 has been shown to inhibit apoptosis. The major aim of this study was to evaluate expression of IL-6 in BE at the protein and mRNA levels. In addition, we tested whether proteins that are associated with IL-6 signaling, phosphorylated signal transducer and activator of transcription 3 and two antiapoptotic proteins, Bcl-x(L) and Mcl-1, are also expressed in the same tissues.Biopsies of duodenum, BE, and squamous epithelium were evaluated by using a human cytokine protein array, ELISA, real-time PCR, and immunohistochemistry.Increased IL-6 levels were found to be secreted from BE tissue compared with duodenum or squamous epithelium from sites adjacent or 5 cm away from the BE lesion. IL-6 mRNA was also elevated in BE compared with duodenum or squamous epithelium in five of seven patients. Immunohistochemical studies confirmed IL-6 expression in intestinal glandular epithelium in BE tissue. Activated signal transducer and activator of transcription 3, Mcl-1, and Bcl-x(L) are present at higher levels in BE glands, with lower levels being found in duodenum or squamous epitheliumThese data, taken together, suggest that elevated IL-6 levels in BE may contribute to the development of apoptosis resistance, thereby placing this epithelium at higher risk of developing malignancy.

PubMed ID: 15041721 Exiting the NIEHS site

MeSH Terms: No MeSH terms associated with this publication

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