Sarah J. Skuli

The paper identifies LDB1-dependent enhancer connectivity as critical for T-cell leukemia subtypes and reveals a metabolic vulnerability exploitable by statins.

This study uses single-cell multiomic analysis to reveal genotype-immunophenotype relationships and clonal evolution in NPM1-mutant AML across disease stages.

This study shows pitavastatin overcomes venetoclax resistance in AML by depleting GGPP, inducing apoptosis through PUMA upregulation and MCL-1 reduction, and suppressing mitochondrial metabolism.

This study identifies GGPP, a mevalonate pathway byproduct, as critical for chemoresistance in TP53mut AML through ROS regulation and mitochondria stress response, suggesting statin-based therapies could be effective.