期刊
JOURNAL OF CELL COMMUNICATION AND SIGNALING
卷 10, 期 3, 页码 207-216出版社
SPRINGER
DOI: 10.1007/s12079-016-0343-9
关键词
CCN1; CCN2; CCN3; CCN4; CCN5; Pancreatic cancer; Patient derived xenograft; Genetically engineered mice model
类别
资金
- Kansas City Area Life Science
- Department of Veterans Affairs [5I01BX001989-03, 1I01BX001002-04]
- KUMC Van Goethem Family Endowed Funds
Decades of basic and translational studies have identified the mechanisms by which pancreatic cancer cells use molecular pathways to hijack the normal home-ostasis 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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