A5088331078- Acute Myeloid Leukemia Research
- Computational Drug Discovery Methods
- Bioinformatics and Genomic Networks
- Protein Degradation and Inhibitors
- Genomics and Chromatin Dynamics
- Chronic Myeloid Leukemia Treatments
- Cancer Genomics and Diagnostics
- Chronic Lymphocytic Leukemia Research
- Histone Deacetylase Inhibitors Research
- Multiple Myeloma Research and Treatments
- Retinoids in leukemia and cellular processes
- Epigenetics and DNA Methylation
University of Rome Tor Vergata
2022-2025
About 40% of relapsed or non-responder tumors exhibit therapeutic resistance in the absence a clear genetic cause, suggesting pivotal role intracellular communication. A deeper understanding signaling pathways rewiring occurring resistant cells is crucial to propose alternative effective strategies for cancer patients. To achieve this goal, we developed novel multi-step strategy, which integrates high sensitive mass spectrometry-based phosphoproteomics with network-based analysis. This...
Abstract The insertion site of the internal tandem duplications (ITDs) in FLT3 gene affects sensitivity to tyrosine kinase inhibitors (TKIs) therapy acute myeloid leukemia (AML). Patients with ITD domain lack effective therapeutic options. Here, identify genotype-driven strategies increasing TKI efficacy, we developed SignalingProfiler , a strategy supporting integration high-sensitive mass spectrometry-based (phospho)proteomics, RNA sequencing datasets literature-derived signaling networks....
BCR::ABL1 drives chronic myeloid leukemia (CML) disease and treatment, as revealed by the success of tyrosine kinase inhibitor (TKI) therapy. However, additional poorly characterized molecular pathways, acting independent mechanisms, play crucial roles in CML, contributing to leukemic stem cells (LSCs) persistence, TKI resistance progression. Here, combining high sensitive mass spectrometry (MS)-based phosphoproteomics with SignalingProfiler pipeline, we obtained two signaling maps offering...
Currently, the identification of patient-specific therapies in cancer is mainly informed by personalized genomic analysis. In setting acute myeloid leukemia (AML), patient-drug treatment matching fails a subset patients harboring atypical internal tandem duplications (ITDs) tyrosine kinase domain FLT3 gene. To address this unmet medical need, here we develop systems-based strategy that integrates multiparametric analysis crucial signaling pathways, and transcriptomic data with prior...
Currently, the identification of patient-specific therapies in cancer is mainly informed by personalized genomic analysis. In setting acute myeloid leukemia (AML), patient-drug treatment matching fails a subset patients harboring atypical internal tandem duplications (ITDs) tyrosine kinase domain FLT3 gene. To address this unmet medical need, here we develop systems-based strategy that integrates multiparametric analysis crucial signaling pathways, and transcriptomic data with...
Currently, the identification of patient-specific therapies in cancer is mainly informed by personalized genomic analysis. In setting acute myeloid leukemia (AML), patient-drug treatment matching fails a subset patients harboring atypical internal tandem duplications (ITDs) tyrosine kinase domain FLT3 gene. To address this unmet medical need, here we develop systems-based strategy that integrates multiparametric analysis crucial signaling pathways, and transcriptomic data with prior...
Summary Currently, the identification of patient-specific therapies in cancer is mainly informed by personalized genomic analysis. In setting acute myeloid leukemia (AML), patient-drug treatment matching fails a subset patients harboring atypical internal tandem duplications (ITDs) tyrosine kinase domain FLT3 gene. To address this unmet medical need, here we develop systems-based strategy that integrates multiparametric analysis crucial signaling pathways, and transcriptomic data with...
Background: Internal tandem duplications (ITDs) in FLT3 gene occurs about 30% of patients with a de novo AML diagnosis and are generally associated poor prognostic outcomes. The different FLT3-ITD insertion site impacts the sensitivity to tyrosine kinase inhibitors (TKIs) treatment, influencing patients’ clinical outcome. Specifically, ITD domain (TKD) is chemoresistance, relapse lower overall survival. Aims: Our work aims elucidate molecular mechanisms driving cells (TKIs). Additionally, we...
Currently, the identification of patient-specific therapies in cancer is mainly informed by personalized genomic analysis. In setting acute myeloid leukemia (AML), patient-drug treatment matching fails a subset patients harboring atypical internal tandem duplications (ITDs) tyrosine kinase domain FLT3 gene. To address this unmet medical need, here we develop systems-based strategy that integrates multiparametric analysis crucial signaling pathways, and transcriptomic data with...
Summary Internal tandem duplications (ITDs) in the FLT3 gene are frequently identified and confer a poor prognosis patient affected by acute myeloid leukemia (AML). The insertion site of ITDs significantly impacts sensitivity to tyrosine kinase inhibitors (TKIs) therapy, affecting patient’s clinical outcome. To decipher molecular mechanisms driving different TKIs therapy FLT3-ITD mutation, we used high-sensitive mass spectrometry-based (phospho)proteomics deep sequencing. Here, present novel...