Targeting H3K36 Methylation in Acute Myeloid Leukemia

• Applicant: Dr. Michael Hötker
• Subject Area: Hematology, Oncology
• Term: since 2025
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 569946953

During the development of cancer, healthy cells lose their identity and differentiation to activate previously silenced programs and start proliferating uncontrollably. A key player in maintaining cellular identity is histone methylation, which modulates the activity of non-coding, regulatory DNA elements. In acute myeloid leukemia (AML), enzymes controlling specific histone modifications are frequently over-expressed, and disrupting these modifications impacts AML cell growth. In this project, we aim to dissect how AML depends on intact histone methylation, which enzymes and genomic loci are involved, and how we could therapeutically leverage these insights. To this end, we will perturb histone methylation in cell lines and patient samples, taking into account the heterogeneity of AML. Additionally, we will analyze healthy blood stem cells. Together, this will allow us to understand how AML cells hijack physiological epigenetic mechanisms. By dissecting the downstream consequences of epigenetic changes, we aim to understand how malignant programs are established and stabilized, and which molecular players are involved. These insights will help us identify new biomarkers and potential therapeutic targets.

• DFG Programme: Research Grants