Aberrant signaling pathways in pancreatic cancer. opportunities for targeted therapeutics

Alixanna Norris, Murray Korc

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The cell type that gives rise to pancreatic ductal adenocarcinoma (PDAC) has not been clearly delineated. PDAC, the most common pancreatic tumor, is currently the fourth leading cause of cancer death. Specific molecular alterations have been shown to correlate with discrete pathological stages of pancreatic tumorigenesis and contribute to specific features of PDAC. Additional alterations suggested to play a role in PDAC include the overexpression of a number of important growth factors and their corresponding high affinity tyrosine kinase receptors, transforming growth factor beta (TGF-β) isoforms, Hedgehog signaling components, the Wnt signaling pathway, the cell cycle regulatory pathway, and nuclear effectors such as Notch, NFκB, and Stat3. Several mouse models of PDAC are produced in which a key component has been the expression of oncogenic K-ras in the pancreas through its own endogenous promoter. In spite of tremendous progress in understanding the pathobiology of PDAC, very little progress has been made with respect to impacting the 5-year survival rates of PDAC patients. Combinational regimens in conjunction with standard chemotherapy may need to be devised, based on the specific molecular alterations that are delineated in a particular patient's cancer. This personalized combinatorial targeted approach may offer a new ray of hope to patients with PDAC.

Original languageEnglish (US)
Title of host publicationHandbook of Cell Signaling, 2/e
PublisherElsevier Inc.
Pages2783-2798
Number of pages16
Volume3
ISBN (Print)9780123741455
DOIs
StatePublished - Dec 1 2010

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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  • Cite this

    Norris, A., & Korc, M. (2010). Aberrant signaling pathways in pancreatic cancer. opportunities for targeted therapeutics. In Handbook of Cell Signaling, 2/e (Vol. 3, pp. 2783-2798). Elsevier Inc.. https://doi.org/10.1016/B978-0-12-374145-5.00324-7