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 language||English (US)|
|Title of host publication||Handbook of Cell Signaling, 2/e|
|Number of pages||16|
|State||Published - Dec 1 2010|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)