PL EN


Preferences help
enabled [disable] Abstract
Number of results
2005 | 53 | 5 | 381-387
Article title

Signal transduction in human pancreatic cancer: roles of transforming growth factor beta, somatostatin receptors, and other signal intermediates

Title variants
Languages of publication
EN
Abstracts
EN
Pancreatic cancer is a devastating disease because of the lack of early detection markers and effective treatments. It is the fourth leading cause of cancer-related death in western countries, including the United States. The mechanisms of pancreatic cancer progression remain unknown. Transforming growth factor beta (TGF-beta), a multifunctional cytokine, regulates cell growth and differentiation in healthy tissues, yet fails to do so in pancreatic cancer. Alterations of the TGF-beta and TGF-beta receptor/Smad signal transduction pathway have been implicated in pancreatic cancer. Furthermore, both the TGF-beta receptor and Smad proteins interact with a variety of cellular signal pathways, such as the somatostatin receptors (SSTRs), ERK1/2, and Wnt signal transduction cascades. This suggests that pancreatic cancer is a multi-gene-controlled malignancy and that effective treatments for pancreatic cancer should be aimed at multiple targets. In this review, we summarized the major signal intermediates involved in pancreatic cancer signal transduction pathways and specifically discussed how alterations in the regulatory functions of TGF-beta and Smad proteins allow for pancreatic carcinogenesis.
Publisher

Year
Volume
53
Issue
5
Pages
381-387
Physical description
Contributors
author
author
author
author
author
author
References
Document Type
REVIEW
Publication order reference
Min Li, Molecular Surgeon Research Center, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77021, USA
Identifiers
YADDA identifier
bwmeta1.element.element-from-psjc-8685c04b-fcc9-32f1-8e31-4742e13e2b63
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.