Thomas Fischer

The paper uses proteomics to identify metabolic vulnerabilities in FLT3-ITD AML cells, showing lipid restriction restores midostaurin sensitivity.

This study shows that NLRP3 inflammasome activation drives JAK2V617F mutant myeloproliferative neoplasms by promoting inflammation, platelet production, and fibrosis, and that its inhibition can reverse disease features.

This study investigates how kinase inhibitors reshape the immunopeptidome in CML by altering HLA-I peptide presentation through three molecular mechanisms.

Pyjacker detects enhancer hijacking in AML, identifying MNX1 activation via 7q deletion as a novel oncogenic mechanism.

The paper identifies BCR::ABL1-independent survival mechanisms in CML using phosphoproteomics and computational analysis, highlighting FLT3 as a therapeutic target for TKI-resistant cases.

This study develops a systems-based strategy to predict drug sensitivity in FLT3-ITD AML by integrating genomic, transcriptomic data with a prior-knowledge signaling network.

The paper develops and evaluates mathematical models to predict white blood cell dynamics during cytarabine treatment in AML, finding that different models yield similar accuracy and identifying a new pharmacodynamic hypothesis.