David M. Ross

This study uses a new long-read sequencing method to genotype mutations in single cells from MPN patients, revealing how mutations drive disease progression to AML.

The paper uses a discrete-parameter ABC-PMC framework to infer the cellular origin of chronic myeloid leukemia, finding that the stem cell compartment is most likely the source.

This study shows that mitochondrial DNA mutations are linked to better responses to kinase inhibitor therapy and reduced oxidative phosphorylation in CML patients.

This study identifies CD44 and FAK as therapeutic targets to reverse adhesion-mediated drug resistance in AML by developing an in-vitro BMME model and testing their synergistic effects.