Abstract
Pancreatic ductal adenocarcinoma is a dismal disease with a median survival of less than 6 months and an overall 5-year survival rate less than 1% . This bad prognosis is due to early lymphatic and hematogenic dissemination. Effective therapies for locally advanced or metastatic tumors are very limited and curatively resected patients experience relapse in over 80% of cases. Together, these findings reflect the aggressive biology of the disease. Here, we describe molecular mechanisms leading to unrestrained proliferation, insensitivity to growth inhibitory signals, evasion of apoptosis, limitless replicative potential, tissue invasion, metastasis and sustained angiogenesis. Potential therapeutic targets are highlighted.
- Pancreatic ductal adenocarcinoma
- INK4a
- K-RAS
- SMAD4
- TP53
- NF-κB
- PI3K
- SKP2
- RB
- p27Kip1
- cell cycle
- angiogenesis
- metastasis
- proliferation
- apoptosis
- epigenetic gene regulation
- miRNA
- epithelial-mesenchymal transition
- chemotaxis
- sonic hedgehog
- review
Footnotes
- Received January 9, 2008.
- Revision received March 18, 2008.
- Accepted March 24, 2008.
- Copyright© 2008 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved