Valeria Bica

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

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

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.