| Literature DB >> 27541366 |
Sushanta K Banerjee1,2,3,4, Gargi Maity5,6, Inamul Haque5,7, Arnab Ghosh5,7, Sandipto Sarkar5,8, Vijayalaxmi Gupta5,7, Donald R Campbell9, Daniel Von Hoff10, Snigdha Banerjee11,12.
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.Entities:
Keywords: CCN1; CCN2; CCN3; CCN4; CCN5; Genetically engineered mice model; Pancreatic cancer; Patient derived xenograft
Year: 2016 PMID: 27541366 PMCID: PMC5055500 DOI: 10.1007/s12079-016-0343-9
Source DB: PubMed Journal: J Cell Commun Signal ISSN: 1873-9601 Impact factor: 5.782