Drs. Naran, Abrams, de Oliveira, and Hughes of the Section of Gastrointestinal Surgery,
Department of Surgery at the University of Pittsburgh have evaluated the role of non-acidic
reflux and the molecular impact of the reflux contents to establish pathophysiologically
the Barrett's esophagus [
1
]. Of primacy to the hypothesis, the authors established the role of bile salts to
elicit subsequent alterations in cell surface expression of CD95 (Fas/Apo-1). The
authors further explored the differential of the normal esophageal squamous epithelium
versus that of Barrett's columnar epithelium to sensitivity of CD95-mediated apoptosis.
In the article recently published in the Journal of Surgical Research [
1
], the authors note that bile salt exposure sensitizes esophageal squamous cells to
CD95-mediated apoptosis. Of key differentiation, this response is differentiated from
that of normal columnar epithelial cells and, thus, may be hypothetically indicative
of the pathogenesis of the Barrett's esophagus.To read this article in full you will need to make a payment
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References
- Bile salts differentially sensitize esophageal squamous cells to CD95 (Fas/Apo-1 receptor) mediated apoptosis.J Surg Res. 2010; (in press)
- Fas/APO-1 (CD95) is not translocated to the cell membrane in esophageal adenocarcinoma.Cancer Res. 1997; 57: 5571
- Matrix metalloproteinase-7 is expressed by pancreatic cancer precursors and regulates acinar-to-ductal metaplasia in exocrine pancreas.J Clin Invest. 2002; 109: 1437
- Induction of apoptosis by cancer chemotherapy.Exp Cell Res. 2000; 256: 42
- Shared pathways: Death receptors and cytotoxic drugs in cancer therapy.Pathol Oncol Res. 2001; 7: 95
- Targeting the protein kinase C family: Are we there yet?.Nat Rev Cancer. 2007; 7: 554
Article info
Publication history
Published online: June 30, 2010
Received:
May 10,
2010
Identification
Copyright
© 2011 Elsevier Inc. Published by Elsevier Inc. All rights reserved.