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Human pancreatic cancer progression: an anarchy among CCN-siblings
Sushanta K Banerjee1,2,3,4, Gargi Maity5,6, Inamul Haque5,7
1Cancer Research Unit, VA Medical Center, Kansas City, 4801 Linwood Blvd, Kansas City, MO, 64128, USA. sbanerjee2@kumc.edu.
Abstract:
Decades of basic and translational studies have identified the mechanisms by which pancreatic cancer cells use molecular pathways to hijack the normal homeostasis of the pancreas, promoting pancreatic cancer initiation, progression, and metastasis, as well as drug resistance. These molecular pathways were explored to develop targeted therapies to prevent or cure this fatal disease. Regrettably, the studies found that majority of the molecular events that dictate carcinogenic growth in the pancreas are non-actionable (potential non-responder groups of targeted therapy). In this review we discuss exciting discoveries on CCN-siblings that reveal how CCN-family members contribute to the different aspects of the development of pancreatic cancer with special emphasis on therapy.
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