Our research
A major task for our group is to define how the AML epigenome is dysregulated in AML, how this leads to leukemia transformation and how this can be used for precision medicine and for improving the treatment of the disease. We currently focus on advanced integrated epigenetic analyses describing the higher order of chromatin and we also explore the role of long non-coding RNAs (lncRNAs) in AML.
To understand the epigenetic dysfunctions in AML in a more complex molecular perspective, we explore the interplay between the epigenome with the AML genome, transcriptome, proteome and drug sensitivity using genome wide multiomic characterization in large AML cohorts. We then use gene editing techniques such as CRISPR-Cas9 and dCas9 to individually validate molecular features that are most likely to be important for AML transformation and treatment. As AML cell populations are heterogenous we also study cell heterogeneity with a focus on epigenetic changes using several types of in single cell analyses.
We are especially interested in the epigenetic effects behind the synergism between azacytidine and venetoklax and we study this with a combination of epigenetic and proteomics studies. Using larger population-based cohorts, we also study the role of clonal hematopoeisis with focus on mutations in epigenetically regulating genes.
In addition to our epigenetic approach, we have a particular interest in therapy-related AML as well as acute promyelocytic leukemia that we study from an epidemiological as well as a molecular perspective.
