Olaf Witt

This study shows that standard therapies for paediatric BRAF-V600E glioma induce senescence, which can be targeted by BCL-xL inhibitors to prevent tumour regrowth.

This study uses pan-cancer phosphoproteomics to identify therapeutic targets and improve precision oncology by analyzing 1,998 tumor samples and developing new scores for kinase activity and immune response.

This study develops an ex vivo drug sensitivity testing platform for rare solid tumors and finds that high in vitro sensitivity correlates with clinical benefit and progression-free survival.

This paper creates a multi-omics atlas of human hindbrain development, revealing cellular diversity, regulatory programs, and disease relevance.

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 identifies SMARCAL1 as a novel predisposition gene for osteosarcoma by analyzing germline variants in DNA damage repair genes across childhood cancer cases.

This study identifies FGFR alterations in pediatric gliomas, their association with specific histologies, and their response to targeted therapies.

The paper uses single-cell technologies to show that large-scale chromosomal aberrations drive medulloblastoma initiation, while single-gene oncogenic events like MYC contribute to progression and therapy resistance.

This study identifies GLRX3 as a vulnerability in Ewing sarcoma driven by EWSR1::FLI1 fusion oncoproteins, showing its role in oxidative stress and iron homeostasis and potential therapeutic targeting.

This study identifies cell-state plasticity as a driver of heterogeneity in Group 3/4 medulloblastomas, showing that transcription factor perturbation can redirect tumor cells along different differentiation trajectories.

The paper identifies ROS1 fusions in various glioma types through genomic and transcriptomic analysis, showing they are not restricted to specific subtypes.