Jan‐Henning Klusmann

This study identifies IGF2BP1 as a regulator of mitotic integrity in CRC, showing that its inhibition creates a therapeutic vulnerability that synergizes with paclitaxel.

This study identifies functional enhancer dependencies in pediatric AML using an integrative approach, revealing H-ME as an RNA-independent regulator of MYB.

This study identifies SNHG29 and IGF2BP1 as a lineage-specific oncogenic circuit in AMKL, showing their dependency and therapeutic vulnerability.

This study identifies DLK1 as a GATA1s-driven dependency in Down syndrome-associated myeloid leukemia, showing it as a therapeutic target with preclinical efficacy in PDX models.

The paper introduces a PDX platform for pediatric cancers, providing in vivo drug testing models and molecular data to aid in therapy development.

The paper develops patient-derived AML PDX models that replicate primary AML biology and include subgroups lacking existing models, showing reduced leukemia growth after long-term chemotherapy.

This study identifies TRIP13 as a developmentally restricted dependency in NUP98::KDM5A+ pediatric AML, showing that its inhibition reactivates TP53 and kills leukemic cells.

The paper examines the transcriptional evolution of myeloid leukaemia in Down syndrome by analyzing single-cell RNA sequencing data from patient samples and fetal tissues.