Edward C. Stites

The paper develops a mathematical model of RAF activation modulated by 14-3-3 proteins, showing that weak binding stabilized by avidity explains experimental observations of RAF activation upon 14-3-3 overexpression.

This study shows that increased wild-type KRAS protein dosage in KRAS-mutant lung cancer drives tumor growth and drug resistance, with vascular changes mediated by mTOR pathway activation.

This paper uses a computational systems pharmacology model to analyze KRAS G12C inhibitors, identifying potential strategies to improve their effectiveness and understanding resistance mechanisms.