Kirsten L. Bryant

Folate metabolism in tumor-associated macrophages drives immunosuppressive function to promote tumor growth

Tumor-associated macrophages (TAMs) promote tumor growth, inhibit effector lymphocytes, and induce resistance to immune checkpoint inhibitors (ICI). Therapies designed to deplete TAMs have had little success in the clinic, and strategies aimed to repolarize immunosuppressive TAMs to pro-inflammatory states have struggl...

Abstract A111: Understanding the interplay between ULK1/2 signaling and the RAS MAPK pathway

Pancreatic ductal adenocarcinoma (PDAC) is dependent on mutant KRAS and elevated autophagy for growth. Previously, we and others demonstrated that pharmacological inhibition of the KRAS ERK-MAPK pathway caused increased autophagic flux. Targeting this increased autophagic flux with inhibitors that block autophagic pr...

Survivin Promotes the Formation of a Microtubule-Based Glycolytic Hub

Abstract A047: Mechanistic dissection and inhibitor targeting of nutrient scavenging in pancreatic cancer

Mutational activation of the KRAS oncogene occurs in over 90% of pancreatic ductal adenocarcinoma (PDAC) patients, and plays a crucial role in tumor initiation, progression, and tumor maintenance. Historically considered undruggable, there has recently been a surge in efforts to develop and improve drugs that target...

Concurrent AXL Inhibition Enhances RAS and ERK Inhibitor Efficacy in KRAS-mutant Pancreatic and Lung Cancer

Combined treatment with the AXL inhibitor bemcentinib together with the RAS(ON) multi-selective tri-complex inhibitor RMC-7977 (RASi) or the ERK-selective inhibitor SCH772984 (ERKi) significantly enhanced growth suppression in human KRAS-mutant pancreatic and lung cancer models.