Differentiation therapy in Acute Myeloid Leukemia: The interplay between metabolism and histone epigenetics defines stemness

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Acute Myeloid Leukemia (AML) is a heterogeneous hematologic malignancy marked by the uncontrolled proliferation of abnormal myeloid precursor cells, with impaired differentiation and metabolic shifts, underscoring the need to target epigenetic and metabolic regulators in its treatment. Proteins, histone PTMs and metabolites collectively define the molecular phenotype, i.e. the cellular differentiation state, and non-terminally differentiated myeloid cells are the main drivers in AML. The success of Menin inhibitors (e.g. Revumenib) arises from their ability to disrupt the interaction Menin-KMT2A, which regulates H3K4me. This triggers AML cell differentiation, briefly increasing cell counts before ultimately leading to cell death and remission. ProGenTomics has developed a novel biomolecular framework wherein histone PTMs, protein expression, and metabolism form an "energy-information axis", with histones acting as signal integrators, that regulate gene activity based on the cell’s metabolic state. Using a multi-omics MS-based approach, we profiled the histonome, metabolome and proteome from a single cell pellet. This workflow was implemented across 18 genetically distinct AML cell lines, generating a coherent dataset, that facilitates the identification of key molecular regulators of AML differentiation therapy. By applying our multi-omics workflow to a timelapse design, we will study causation during AML differentiation within the framework of our newly established picture.

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