https://orcid.org/0000-0003-2869-1571
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ABSTRACT
Pancreatic cancer is characterized by extreme therapeutic resistance. In pancreatic cancers harboring high-risk genomes, we describe that cancer cell-neutrophil signaling circuitry provokes neutrophil-derived transmembrane (tm)TNF-TNFR2 interactions that dictate inflammatory polarization in cancer-associated fibroblasts and T-cell dysfunction – two hallmarks of therapeutic resistance. Targeting tmTNF-TNFR2 signaling may sensitize pancreatic cancer to chemo±immunotherapy.
Disclosure statement
Dr. Datta receives research funding from Cantargia AB Inc., unrelated to the context of this work.
Additional information
Funding
The work was supported by the American College of Surgeons National Institutes of Health [T32 CA211034]; National Institutes of Health [UL1TR002736]; Pancreatic Cancer Action Network.