The heat shock response in pancreatitis that is activated via HSP70 protects acinar cells through multiple simultaneous mechanisms. It inhibits trypsinogen activation and modulates NF-κB signaling to limit acinar cell injury. On the other hand, HSP70 is overexpressed in pancreatic cancer and is hijacked by the cellular machinery to inhibit apoptosis. Inhibition of HSP70 in pancreatic cancer by a novel compound, Minnelide, has shown considerable clinical promise.
Bibliographical noteFunding Information:
This study was funded by NIH grants R01-CA170946 and R01-CA124723 (to AKS); Authors also want to acknowledge the intra-mural support from Sylvester Comprehensive Cancer Center. The University of Minnesota has a patent for Minnelide™ (which has been licensed to Minneamrita Therapeutics LLC, Moline, IL). AS has ownership interests (including patents) and is a consultant/advisory board member for Minneamrita Therapeutics LLC. Dr Sulagna Banerjee is a consultant for Minneamrita Therapeutics, licensee of the intellectual property (Minnelide) being described in the study. The other authors have nothing to disclose.
© 2017 Wiley Periodicals, Inc.
- pancreatic cancer