Francesca Sacco

Organelle proteomics reveals novel metabolic vulnerabilities in FLT3-ITD cells

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

Targeting Kinases to Reshape the Immunopeptidome landscape in Chronic Myeloid Leukemia

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

PatientProfiler: A network-based approach to personalized medicine

PatientProfiler integrates multi-omic data to generate patient-specific mechanistic models and prognostic biomarkers for breast cancer.

Phosphoproteomics reveals novel BCR::ABL1-independent mechanisms of resistance in chronic myeloid leukemia

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.

SignalingProfiler 2.0: a network-based approach to bridge multi-omics data to phenotypic hallmarks

SignalingProfiler 2.0 integrates proteogenomic data with causal networks to generate mechanistic signaling models that recapitulate drug-perturbed phenotypes in breast cancer cells.

COVID-19 Disease Map, a computational knowledge repository of SARS-CoV-2 virus-host interaction mechanisms

The paper describes the development of a computational knowledge repository, the COVID-19 Disease Map, which curates SARS-CoV-2 virus-host interaction mechanisms and provides tools for their analysis and application.

Myo-REG: a portal for signaling interactions in muscle regeneration

Myo-REG integrates and curates molecular interactions and signaling pathways involved in muscle regeneration, providing a web portal for exploring cell-cell and intracellular interactions.

In vivo phosphoproteomics reveals pathogenic signaling changes in diabetic islets

The paper uses phosphoproteomics to identify signaling changes in diabetic islets, revealing GSK3's role in PDX1 and insulin secretion.

Skeletal muscle fibro-adipogenic progenitors of dystrophic mice are insensitive to NOTCH-dependent regulation of adipogenesis

This study shows that NOTCH signaling inhibits adipogenesis in wild-type FAPs but not in mdx FAPs, with TNF-α restoring NOTCH sensitivity in mdx FAPs.