Frank P. McCormick

This study identifies DIRAS3 as a tumor suppressor that inhibits diverse oncogenic KRAS variants through a specific inhibitory interface, with a mimetic showing broad suppression of KRAS-driven signaling.

This study identifies ELV-3111, a Type 1 RAF inhibitor that selectively suppresses MAPK and tumor growth by exploiting distinct binding kinetics, showing efficacy in RAS-mutant and BRAF-mutant models.

This study shows that a dual inhibitor of KRASG12C in both ON and OFF states more effectively suppresses tumor growth than an OFF-specific inhibitor by reducing PI3K-AKT activation.

This paper designs molecular glues that stabilize the 14-3-3/C-RAF autoinhibited complex, showing selectivity and functional effects in biophysical and cell assays.

This study develops PNA oligomers targeting KRAS G12D mutations with cell-penetrating peptides, showing selective repression of mutant mRNA and protein in cells and efficacy in vivo.

This study validates the palmitoylation cycle as a therapeutic target in NRAS-mutant cancers by showing that inhibiting ABHD17 reduces tumor growth and synergizes with MEK inhibitors.

This study uses deep mutational scanning to analyze KRAS variants, identifying gain- and loss-of-function mechanisms and their impact on oncogenic activity.

The paper analyzes LZTR1 loss-of-function mutants in fruit flies and mice, showing dependency on RIT1 orthologs and haplosufficiency in mice.

The paper quantifies ERK activity in RAS-mutant cells and finds that mutant KRAS isoforms produce similar ERK output ranges despite differing biochemical activity, due to pathway-level rescaling mechanisms.

The paper introduces an orthogonal CRISPR/Cas screen to systematically activate one gene while knocking out another, enabling the identification and directionality of genetic interactions in human cancer cells.