The McFall Lab
PUBLICATIONS
Mutant and Wild-Type RAS Cross-talk and Stoichiometric Deficiencies Are Determinants of Sensitivity to Targeted Therapies in KRAS G12R Pancreatic Ductal Adenocarcinoma
It was determined that KRAS G12R is unable to bind key regulators in its signaling pathway, making it possible to target tumors with MEK inhibitors with an autophagy inhibitor. A small study of 8 patients with a G12R mutation were treated with this combination therapy and 5 had progression-free survival of at least six months. One patient had tumor regression by 83% and stayed stable for nearly nine months.
Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors
KRAS G13D exhibits a paradoxical sensitivity to the EGFR inhibitor cetuximab in colorectal cancer. This study describes the mechanism underlying this unique sensitivity, driven by impaired GAP binding and dependence on upstream EGFR signaling.
Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach
RAS mutations were previously regarded as a biomarker for resistance to EGFR inhibitors in colorectal cancer. This study highlights the importance of understanding the interactions of the individual mutant RAS proteins and explores NF1 binding as a possible biomarker for EGFR inhibitor sensitivity.
Transcriptomic-Based Microenvironment Classification Reveals Precision Medicine Strategies for Pancreatic Ductal Adenocarcinoma
Transcriptomic profiling defines a distinct subgroup of PDAC patients that may benefit from immunotherapeutic strategies based on their TME subtype and provides a framework to select patients for prospective clinical trials investigating precision immunotherapy in PDAC.