Human pancreatic cancer progression: an anarchy among CCN-siblings
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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.
KeywordsCCN1 CCN2 CCN3 CCN4 CCN5 Pancreatic cancer Patient derived xenograft Genetically engineered mice model
We would like to thank other members of our cancer research unit for valuable and helpful comments on this manuscript. We would also like to thank LaCoiya Harris for editing and organizing this manuscript. This work was supported by the Kansas City Area Life Science grant award (SKB), Merit review grant from Department of Veterans Affairs (SKB, 5I01BX001989-03 and SB,1I01BX001002-04), and KUMC Van Goethem Family Endowed Funds (SKB).
Snigdha Banerjee and Sushanta K. Banerjee performed the literature search and wrote the manuscript. Inamul Haque, Gargi Maity, Vijayalaxmi Gupta, Sandipto Sarkar and Arnab Ghosh revised it critically for important intellectual content. Donald Campbell and Daniel Von Hoff provided expert comments and editing.
Compliance with ethical standards
Conflicts of interest
The authors declare no conflict of interest.
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