bioRxiv [Preprint], Feb 02, 2026

In this preprint, we developed a CRISPR/Cas9-engineered humanized model of familial GATA2-deficient myelodysplastic syndrome (MDS) to define how STAG2 loss cooperates in disease progression. Genome editing of primary human hematopoietic stem and progenitor cells followed by xenotransplantation demonstrates that STAG2 loss enhances stem cell persistence and myeloid skewing in the context of GATA2 deficiency. Single-cell analyses identify transcriptional programs linked to stemness and inflammatory signaling, providing mechanistic insight into high-risk GATA2-mutant MDS evolution.

Cancer Discovery, Dec 10, 2025

In this recently published study, we investigated the role of the NUP98-NSD1 fusion oncogene in pediatric acute myeloid leukemia (AML), demonstrating that its expression in human hematopoietic stem and progenitor cells leads to leukemic transformation. We further elucidated that the oncogenic potential of NUP98-NSD1 is influenced by the ontogeny of the cells, highlighting the importance of developmental context in leukemia pathogenesis.

Blood Cancer Discovery, May 02, 2025

We recently wrote a review on overcoming resistance to targeted and immune therapies in B-cell acute lymphoblastic leukemia (B-ALL), highlighting rational combination strategies aimed at improving patient outcomes. The article emphasizes integration of targeted therapies, such as tyrosine kinase inhibitors and venetoclax, with immunotherapies like bispecific antibodies, antibody-drug conjugates, and CAR T-cells. It discusses mechanisms of resistance, including antigen escape and signalling pathway adaptations, and outlines novel combination approaches to enhance therapeutic efficacy and durability, significantly advancing translational hematology research