Matthew Froid

The paper shows that targeted therapy resistance in cancer selects for cells with higher phenotypic plasticity, which enhances their ability to adapt to other stressors and promotes metastasis.

This paper uses an agent-based model to simulate how different treatment-free intervals during T-cell engager exposure affect T cell exhaustion and tumor control in B-ALL.

This study develops a computational model of the AML bone marrow microenvironment and shows that combining TKIs with miR-126 inhibition can overcome treatment resistance by disrupting the protective vascular niche.