Molecular Therapeutics: Pancreatic Cancer
© 2016 by John Wiley & Sons, Inc. All rights reserved. As we learn more about the molecular underpinnings of pancreatic cancer, we are discovering new growth pathways that present opportunities for treatment. KRAS represents one such target. Activating mutations, found in the majority of pancreatic cancer, activate downstream activators including RAF, MEK, and ERK, and the hedgehog pathway. The PI3 kinase pathway is also frequently activated through the disruption of the PTEN tumor pathway, in turn activating NF-kB and C-MYC. Likewise, the TGF-β pathway acts through SMAD dependent and independent pathways to control MYC expression, affect epithelial-mesenchymal transition, and modify the immune response. Activation of the Notch pathway receptors has also been shown to regulate cell cycle effectors. DNA repair abnormalities may play a role in the rise of pancreatic cancer; these also have implications for treatment. Finally, immunotherapeutic agents are now being developed for use in pancreatic cancer and other treatments. In this chapter, we review each of these molecular pathways and discuss their applicability to pancreatic cancer treatment.
Fogelman, D; Javle, M; Abbruzzese, J
- Targeted Therapy in Translational Cancer Research
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International Standard Book Number 13 (ISBN-13)
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