Sara Hamis

This paper curates a large corpus of mathematical oncology literature using AI, revealing its evolution from cancer biology to therapeutic modeling over 140 years.

The paper develops a model to show phenotypic adaptation drives drug resistance in BRAFV600E-mutant melanoma and suggests intermittent treatments may be more effective.

This paper develops a stochastic model to assess the identifiability of phenotypic adaptation parameters from low-cell-count experiments and shows that cell-to-cell heterogeneity is non-identifiable from population-level data.

The paper quantifies cell dynamics and interactions in neuroblastoma cell cultures under stress, finding that cell-to-cell interactions drive phenotypic adaptation, which accelerates with lower nutrient levels.

This study uses mathematical models to show that spatial factors influence drug response and competition between drug-sensitive and drug-resistant cancer cells.

This paper develops a mathematical model of BRAFV600E-MEK-ERK signaling dynamics to simulate responses to vertical inhibition treatment strategies and identify effective combinations.

Open-source agent-based PhysiCell model of SARS-CoV-2 infection in lung epithelium; version 5 clears virus in about 6 days in simulation, and delayed T cell arrival increases epithelial loss.