In a recent study published in Nature, Ochi et al. used ATAC-seq to profile bone marrow or peripheral blood tumor cells from 1563 newly diagnosed cases of acute myeloid leukemia (AML), resolving the disease into 16 chromatin-accessibility subgroups (the eCHROMA study) with independent prognostic and pharmacological value, most of them invisible to current genetic classification. 1 This chromatin-based framework raises a sharper question: how much of that architecture can actually be engineered by drugs designed to rewrite it?
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Coelho‐Silva et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: