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ShareScienceDaily (Apr. 19, 2010) — Insulin-like growth factor-I (IGF-I) is upregulated in human pancreatic cancer tissues but is not expressed in surrounding non-cancerous tissues. Serum level of IGF-I is elevated in pancreatic cancer patients. Histological analysis has shown that IGF-I receptor (IGF-IR) is positive in the membrane of pancreatic cancer tissues.
These facts suggest that IGF-I acts as a growth factor for pancreatic cancer and inhibition of its action might be a good candidate for molecular therapy of pancreatic cancer. A possible problem is that not all pancreatic cancers produce IGF-I, which might be a reason for ineffective results of its clinical application.
A research team from Japan have proved that inhibition of IGF-IR activity results in a decrease in proliferation and motility of pancreatic cancer cell lines. Their study will be published on April 21, 2010 in the World Journal of Gastroenterology.
Their study indicated that IGF-IR was expressed and played a role in proliferation and motility of pancreatic cancer cell lines. Further analysis of this phenomenon could unveil a new role for a growth factor receptor and its downstream pathway in cancer. One possible mechanism would be that the downstream pathway stimulates its upstream receptor via some unknown molecule, like a retrograde flow.
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The above story is reprinted from materials provided by World Journal of Gastroenterology, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Tomizawa M, Shinozaki F, Sugiyama T, Yamamoto S, Sueishi M, Yoshida T. Insulin-like growth factor-I receptor in proliferation and motility of pancreatic cancer. World Journal of Gastroenterology, 2010; 16 (15): 1854 DOI: 10.3748/wjg.v16.i15.1854
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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