M. Damaghi

The paper investigates how APOBEC3A/B activity influences the evolvability of cancer-associated genes compared to non-cancer genes across humans and bats, finding bimodal mutation patterns and increased cancer heterogeneity.

This study develops an adaptive therapy protocol for PARP inhibitors by combining mathematical modeling and experiments to optimize treatment scheduling and mitigate resistance.

The paper develops a mathematical model showing that rapid oxygen fluctuations favor pseudohypoxia by selecting for constitutive HIF stabilization despite reduced cell fitness.

This study integrates omics data from breast cancer to show that malignancy evolves through genetic fine-tuning rather than de novo pathways in both pre-invasive and invasive stages.

The paper investigates how harsh microenvironments in early breast cancer select for a Warburg phenotype through metabolic and transcriptomic changes.

This study shows that competition between two breast cancer cell lines depends on frequency-dependent interactions, not just growth rates or carrying capacities.

This study investigates whether a cost of resistance is necessary for adaptive therapy to delay cancer progression, finding that cell turnover modulates this requirement depending on tumor growth conditions.

This study uses a mathematical model to show that stable coexistence of different cancer cell phenotypes enhances tumour invasion by allowing complementary traits to work synergistically.

The paper identifies collagen production as an adaptation strategy in acidotic cancer cells, showing correlation with patient survival.

The paper shows that acidic niches in lymph nodes inhibit T-cell effector functions by blocking lactic acid efflux and reducing glycolysis, keeping T-cells in a state of stasis.