Banerjee Sushanta K, Maity Gargi, Haque Inamul, Ghosh Arnab, Sarkar Sandipto, Gupta Vijayalaxmi, Campbell Donald R, Von Hoff Daniel, Banerjee Snigdha
Cancer Research Unit, VA Medical Center, Kansas City, 4801 Linwood Blvd, Kansas City, MO, 64128, USA.
Department of Oncology, University of Kansas Medical Center, Kansas City, Kansas, USA.
J Cell Commun Signal. 2016 Sep;10(3):207-216. doi: 10.1007/s12079-016-0343-9. Epub 2016 Aug 19.
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.
数十年的基础研究和转化研究已经明确了胰腺癌细胞利用分子途径劫持胰腺正常稳态,从而促进胰腺癌起始、进展、转移以及产生耐药性的机制。人们探索这些分子途径以开发靶向疗法来预防或治愈这种致命疾病。遗憾的是,研究发现,决定胰腺致癌性生长的大多数分子事件是不可靶向作用的(靶向治疗的潜在无反应组)。在本综述中,我们讨论了关于CCN家族成员的激动人心的发现,这些发现揭示了CCN家族成员如何在胰腺癌发展的不同方面发挥作用,特别强调了其与治疗的关系。