Jarno Drost

The paper shows that SMARCB1 loss disrupts TF-dependent chromatin priming, revealing lineage-specific regulatory output of BAF complexes is constrained by TF repertoire in ATRT tumors.

The paper uses lineage tracing and single-cell RNA sequencing to show that rhabdoid tumors converge on a limited set of transcriptional states despite clonal diversity.

The paper estimates the timing of genetic driver events and clonal expansion in rhabdoid tumors using whole-genome sequencing data from 97 tumors.

This study shows that hENT inhibition overcomes pyrimidine-driven resistance to DHODH inhibition in SWI/SNF-deficient pediatric cancers.

This study identifies HIF1A as a key inhibitor of VHL null cell fitness and shows that combined VHL/HIF1A inactivation can confer resistance to PROTAC-based therapies.

The paper introduces PIGI, a pathway-informed framework to detect genetic interactions in pediatric cancer, identifying 35 new candidate gene pairs with potential synthetic lethal interactions.

The paper evaluates how the functional avidity of anti-B7H3 CAR-T constructs relates to their ability to trigger effector function against tumors with varying antigen density.

This study shows that single mutations during early oncogenesis can upregulate BTN2A1, enabling Vγ9Vδ2 TCR binding, but full activation requires subsequent phosphorylation of BTN3A1.

The paper identifies prevalent and pathogenic complex structural variations in pediatric solid tumors, linking them to adverse clinical outcomes and potential therapeutic targets.

This paper develops a method to detect tumor-specific gene fusions in pediatric cancer by integrating RNA-seq and WGS, identifying 165 high-confidence fusions and their structural variants.

This study uses CRC organoids to model immune-cancer interactions and assess immunomodulation by co-culturing with cytotoxic T cells.