A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia

Abstract Background About 40% of relapsed or non-responder tumors exhibit therapeutic resistance in the absence of a clear genetic cause, suggesting a pivotal role of intracellular communication. A deeper understanding of signaling pathways rewiring occurring in resistant cells is crucial to propose...

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Main Authors: Valeria Bica, Veronica Venafra, Giorgia Massacci, Simone Graziosi, Sara Gualdi, Gessica Minnella, Federica Sorà, Patrizia Chiusolo, Maria Elsa Brunetti, Gennaro Napolitano, Massimo Breccia, Dimitrios Mougiakakos, Martin Böttcher, Thomas Fischer, Livia Perfetto, Francesca Sacco
Format: Article
Language:English
Published: BMC 2025-04-01
Series:Cell Communication and Signaling
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Online Access:https://doi.org/10.1186/s12964-025-02185-0
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author Valeria Bica
Veronica Venafra
Giorgia Massacci
Simone Graziosi
Sara Gualdi
Gessica Minnella
Federica Sorà
Patrizia Chiusolo
Maria Elsa Brunetti
Gennaro Napolitano
Massimo Breccia
Dimitrios Mougiakakos
Martin Böttcher
Thomas Fischer
Livia Perfetto
Francesca Sacco
author_facet Valeria Bica
Veronica Venafra
Giorgia Massacci
Simone Graziosi
Sara Gualdi
Gessica Minnella
Federica Sorà
Patrizia Chiusolo
Maria Elsa Brunetti
Gennaro Napolitano
Massimo Breccia
Dimitrios Mougiakakos
Martin Böttcher
Thomas Fischer
Livia Perfetto
Francesca Sacco
author_sort Valeria Bica
collection DOAJ
description Abstract Background About 40% of relapsed or non-responder tumors exhibit therapeutic resistance in the absence of a clear genetic cause, suggesting a pivotal role of intracellular communication. A deeper understanding of signaling pathways rewiring occurring in resistant cells is crucial to propose alternative effective strategies for cancer patients. Methods To achieve this goal, we developed a novel multi-step strategy, which integrates high sensitive mass spectrometry-based phosphoproteomics with network-based analysis. This strategy builds context-specific networks recapitulating the signaling rewiring upon drug treatment in therapy-resistant and sensitive cells. Results We applied this strategy to elucidate the BCR::ABL1-independent mechanisms that drive relapse upon therapy discontinuation in chronic myeloid leukemia (CML) patients. We built a signaling map, detailing - from receptor to key phenotypes - the molecular mechanisms implicated in the control of proliferation, DNA damage response and inflammation of therapy-resistant cells. In-depth analysis of this map uncovered novel therapeutic vulnerabilities. Functional validation in patient-derived leukemic stem cells revealed a crucial role of acquired FLT3-dependency and its underlying molecular mechanism. Conclusions In conclusion, our study presents a novel generally applicable strategy and the reposition of FLT3, one of the most frequently mutated drivers of acute leukemia, as a potential therapeutic target for CML relapsed patients.
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spelling doaj-art-00c843e6d0934990ab3bb953d57a2b382025-08-20T03:52:24ZengBMCCell Communication and Signaling1478-811X2025-04-0123111710.1186/s12964-025-02185-0A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemiaValeria Bica0Veronica Venafra1Giorgia Massacci2Simone Graziosi3Sara Gualdi4Gessica Minnella5Federica Sorà6Patrizia Chiusolo7Maria Elsa Brunetti8Gennaro Napolitano9Massimo Breccia10Dimitrios Mougiakakos11Martin Böttcher12Thomas Fischer13Livia Perfetto14Francesca Sacco15Ph.D. Program in Cellular and Molecular Biology, Department of Biology, University of Rome ’Tor Vergata’Ph.D. Program in Cellular and Molecular Biology, Department of Biology, University of Rome ’Tor Vergata’Department of Biology, University of Rome Tor VergataPh.D. Program in Cellular and Molecular Biology, Department of Biology, University of Rome ’Tor Vergata’Department of Biology and Biotechnologies “C. Darwin”, University of Rome La SapienzaSezione di Ematologia, Dipartimento di Scienze Radiologiche ed Ematologiche, Università Cattolica del Sacro CuoreSezione di Ematologia, Dipartimento di Scienze Radiologiche ed Ematologiche, Università Cattolica del Sacro CuoreSezione di Ematologia, Dipartimento di Scienze Radiologiche ed Ematologiche, Università Cattolica del Sacro CuoreTelethon Institute of Genetics and Medicine (TIGEM)Telethon Institute of Genetics and Medicine (TIGEM)Department of Translational and Precision Medicine, Azienda Policlinico Umberto I, Sapienza University of RomeHealth campus for Inflammation, Immunity and Infection (GCI3), University of MagdeburgHealth campus for Inflammation, Immunity and Infection (GCI3), University of MagdeburgHealth campus for Inflammation, Immunity and Infection (GCI3), University of MagdeburgDepartment of Biology and Biotechnologies “C. Darwin”, University of Rome La SapienzaDepartment of Biology, University of Rome Tor VergataAbstract Background About 40% of relapsed or non-responder tumors exhibit therapeutic resistance in the absence of a clear genetic cause, suggesting a pivotal role of intracellular communication. A deeper understanding of signaling pathways rewiring occurring in resistant cells is crucial to propose alternative effective strategies for cancer patients. Methods To achieve this goal, we developed a novel multi-step strategy, which integrates high sensitive mass spectrometry-based phosphoproteomics with network-based analysis. This strategy builds context-specific networks recapitulating the signaling rewiring upon drug treatment in therapy-resistant and sensitive cells. Results We applied this strategy to elucidate the BCR::ABL1-independent mechanisms that drive relapse upon therapy discontinuation in chronic myeloid leukemia (CML) patients. We built a signaling map, detailing - from receptor to key phenotypes - the molecular mechanisms implicated in the control of proliferation, DNA damage response and inflammation of therapy-resistant cells. In-depth analysis of this map uncovered novel therapeutic vulnerabilities. Functional validation in patient-derived leukemic stem cells revealed a crucial role of acquired FLT3-dependency and its underlying molecular mechanism. Conclusions In conclusion, our study presents a novel generally applicable strategy and the reposition of FLT3, one of the most frequently mutated drivers of acute leukemia, as a potential therapeutic target for CML relapsed patients.https://doi.org/10.1186/s12964-025-02185-0Chronic myeloid leukemiaBCR:ABL1-independent resistanceSignaling pathwaysPhosphoproteomicsComputational strategyDrug repurposing
spellingShingle Valeria Bica
Veronica Venafra
Giorgia Massacci
Simone Graziosi
Sara Gualdi
Gessica Minnella
Federica Sorà
Patrizia Chiusolo
Maria Elsa Brunetti
Gennaro Napolitano
Massimo Breccia
Dimitrios Mougiakakos
Martin Böttcher
Thomas Fischer
Livia Perfetto
Francesca Sacco
A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia
Cell Communication and Signaling
Chronic myeloid leukemia
BCR:ABL1-independent resistance
Signaling pathways
Phosphoproteomics
Computational strategy
Drug repurposing
title A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia
title_full A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia
title_fullStr A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia
title_full_unstemmed A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia
title_short A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia
title_sort network based approach to overcome bcr abl1 independent resistance in chronic myeloid leukemia
topic Chronic myeloid leukemia
BCR:ABL1-independent resistance
Signaling pathways
Phosphoproteomics
Computational strategy
Drug repurposing
url https://doi.org/10.1186/s12964-025-02185-0
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