Jonathan Bond

This study investigates how PRC2 depletion in AML affects epigenomic and transcriptional changes, revealing altered chromatin accessibility, H3K27me3 levels, and gene expression patterns that impact cell phenotype and treatment response.

This study identifies enhancer heterogeneity as a driver of transcriptional differences in KMT2A::AFF1 ALL patients, revealing patient-specific enhancer activity at oncogenes.

This paper uses a structure-based model to identify synergistic RAF inhibitor combinations effective against RAS-mutant AML in vitro and in vivo.

This paper develops bi-specific CAR-iNKT cells targeting CD19 and CD133 for KMT2A-rearranged leukemia, showing superior efficacy over CAR-T in eradicating leptomeningeal disease and inducing remission.

The paper assesses whether gene regulatory networks can predict gene sensitivity in cancer cell lines and finds that mRNA abundance is a better predictor than inferred regulatory activity.

The paper identifies that PRC2 loss in T-ALL reduces WNT pathway activity, leading to asparaginase resistance, which can be overcome by proteasome inhibition.