J. DeGregori

The paper shows that marrow-mediated activation of ATM and mTOR increases oxidative phosphorylation, leading to resistance in FLT3 mutant AML cells, and that combining mTOR and FLT3 inhibitors reduces tumor burden.

This study uses in silico experiments to show that mutation rates in sexual populations can evolve higher or lower depending on selection pressures and genetic factors.

This study shows that PU.1 enforces HSC quiescence by repressing protein synthesis and cell cycle genes, preventing clonal expansion during inflammatory stress.

This study shows chronic IL-1β exposure selects for Cebpa-deficient HSPC by promoting myeloid differentiation and repressing stem cell programs, linking chronic inflammation to hematologic disorders.

This paper uses Monte Carlo modeling to show that aneuploid cell frequency peaks after bone marrow transplantation due to reduced purifying selection from population expansion and radiation-induced niche damage.

This study shows that somatic maintenance and longevity influence mutation rate evolution by modulating the cost of somatic mutations through stochastic modeling.

This study shows that inhibiting glutaminase with CB-839 reduces glutathione and increases mitochondrial ROS in AML, leading to apoptosis, and that combining it with pro-oxidant drugs enhances cell death in AML and ALL.

This study uses Monte Carlo modeling to show that the Multi-Stage Model of Carcinogenesis needs modification to explain cancer incidence and stem cell clonality.