“This is a study that identifies a potential vulnerability created by type I IFNs in pancreatic cancer that can be leveraged for what appears to be an effective therapeutic strategy,” said researcher Timothy Donahue from the University of California – Los Angeles, in a mice-based study. Read more . . .
Researchers have uncovered a potential new way to target pancreatic tumors that express high intratumoral interferon signaling (IFN). The team found that high type I IFN signaling is present in a subset of pancreatic tumors and it triggers a decrease in the level of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide hydrogen (NADH) in pancreatic cancer cells, which are vital cofactors in critical metabolic processes.