Fig. 3.
Inhibition of RIP1 does not affect pancreatic tumor growth. a Overall survival of Kras mutant genetically engineered mouse (GEM) model of pancreatic ductal adenocarcinoma (KPP; LSL-KrasG12D/+; p16/p19fl/fl; Pdx1-cre) on continuous Nec-1a treatment (n = 11) and vehicle control (n = 12); log-rank, NS– not significant, p = 0.47. b Tumor volume measurements based on serial ultrasound imaging of tumors in mice from a. c Serum Cxcl1 measurements via Luminex from KPP mice acutely treated (d7) with indicated compounds. d Overall survival of KPP model on continuous RIP1 inhibition with GNE684 (n = 15) and vehicle control (n = 15); log-rank, NS– not significant, p = 0.08. e Tumor volume measurements based on serial ultrasound imaging of tumors in mice from d. f Overall survival of KPP animals that were Ripk1D138N/+ (RIP1 HET, n = 15), Ripk1D138N/D138N (RIP1 KI, n = 15) or Ripk1+/+ (RIP1 WT, n = 21); log-rank, *p = 0.0064