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My research integrates population-based epidemiology, clonal hematopoiesis, and translational gene editing to address relapse and therapeutic resistance in acute myeloid leukemia (AML). I have led nationwide real-world analyses of RUNX1::RUNX1T1-positive AML, demonstrating high remission rates but relapse as the principal driver of mortality and showing that the clinical benefit of gemtuzumab ozagamicin remains limited in routine clinical practice. Furthermore, I have characterized the evolutionary dynamics of therapy-related AML after autologous stem-cell transplantation, revealing that low-frequency clones can expand from sub-percent variant allele fractions to dominant leukemic clones.
Building on this experience, I co-develop a therapeutic platform targeting fusion-driven AML using CRISPR-Cas9 gene editing technologies. This therapeutic approach has been the main focus of my PhD and through mechanistic studies including in vitro and ex vivo validations of the technology, my work now underpins the ongoing lipid nanoparticle-CRISPR program aimed at developing a gene therapeutic approach for relapse-prone or high-risk AMLs.