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Pancreatic Cancer FISH Probes


KRAS is the most frequently mutated gene in pancreatic ductal adenocarcinoma (PDAC). Mutated KRAS alters glucose uptake, glycolytic flux, and glutamine usage to drive tumor genesis, and upregulates autophagy and micropinocytosis to maintain tumor survival.


MET expression, while critical in the developing pancreatic bud of the embryo, drops to very low levels in normal adult pancreatic cells. PC tumors have been shown to overexpress MET, however, which contributes to pathogenesis by driving crosstalk between cancer cells and the surrounding microenvironment.


Both sporadic and inherited CDKN2A mutations are hallmark alterations in PC, with the latter firmly linked to cases of familial origin. These mutations occur early in development of the disease, facilitating tumor progression through downregulation of the cell cycle regulator CDK4/6.


Deletion of the critical tumor suppressor PTEN is a common event in PDAC development. PTEN deficient tumors exhibit classic PDAC mutations, as well as overactivation of NF-κB and its downstream cytokine pathway, both of which are associated with inflammatory response in the tumor microenvironment.


SMAD4, an important regulator of TGF-B signaling, is homozygously deleted in roughly 30% of pancreatic cancers. These deletions set off a complex network of cellular deregulation in PC tumors, affecting cell arrest, apoptosis, invasion, and metastasis.


TP53 is mutated in 70% of pancreatic cancers. Mutations inactivate wild-type p53 function, but can also produce gain-of-function oncogenic characteristics that contribute to cell proliferation, survival and metastasis, including upregulation of PDGFRB.