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15 results on '"Ferrarini, Marina"'

1. In vitro models of the crosstalk between multiple myeloma and stromal cells recapitulate the mild NF-κB activation observed in vivo

Author

Colombo, Federica, Guzzeloni, Virginia, Kizilirmak, Cise, Brambilla, Francesca, Garcia-Manteiga, Jose Manuel, Tascini, Anna Sofia, Moalli, Federica, Mercalli, Francesca, Ponzoni, Maurilio, Mezzapelle, Rosanna, Ferrarini, Marina, Ferrero, Elisabetta, Visone, Roberta, Rasponi, Marco, Bianchi, Marco E., Zambrano, Samuel, and Agresti, Alessandra

Published
2024
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2. Supplementary Figure Legends from Chromogranin A Is Preferentially Cleaved into Proangiogenic Peptides in the Bone Marrow of Multiple Myeloma Patients

Author

Bianco, Mimma, primary, Gasparri, Anna Maria, primary, Colombo, Barbara, primary, Curnis, Flavio, primary, Girlanda, Stefania, primary, Ponzoni, Maurilio, primary, Bertilaccio, Maria Teresa Sabrina, primary, Calcinotto, Arianna, primary, Sacchi, Angelina, primary, Ferrero, Elisabetta, primary, Ferrarini, Marina, primary, Chesi, Marta, primary, Bergsagel, P. Leif, primary, Bellone, Matteo, primary, Tonon, Giovanni, primary, Ciceri, Fabio, primary, Marcatti, Magda, primary, Caligaris-Cappio, Federico, primary, and Corti, Angelo, primary

Published
2023
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3. Data from Chromogranin A Is Preferentially Cleaved into Proangiogenic Peptides in the Bone Marrow of Multiple Myeloma Patients

Author

Bianco, Mimma, primary, Gasparri, Anna Maria, primary, Colombo, Barbara, primary, Curnis, Flavio, primary, Girlanda, Stefania, primary, Ponzoni, Maurilio, primary, Bertilaccio, Maria Teresa Sabrina, primary, Calcinotto, Arianna, primary, Sacchi, Angelina, primary, Ferrero, Elisabetta, primary, Ferrarini, Marina, primary, Chesi, Marta, primary, Bergsagel, P. Leif, primary, Bellone, Matteo, primary, Tonon, Giovanni, primary, Ciceri, Fabio, primary, Marcatti, Magda, primary, Caligaris-Cappio, Federico, primary, and Corti, Angelo, primary

Published
2023
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4. Supplementary Figures S1-S5 from Chromogranin A Is Preferentially Cleaved into Proangiogenic Peptides in the Bone Marrow of Multiple Myeloma Patients

Author

Bianco, Mimma, primary, Gasparri, Anna Maria, primary, Colombo, Barbara, primary, Curnis, Flavio, primary, Girlanda, Stefania, primary, Ponzoni, Maurilio, primary, Bertilaccio, Maria Teresa Sabrina, primary, Calcinotto, Arianna, primary, Sacchi, Angelina, primary, Ferrero, Elisabetta, primary, Ferrarini, Marina, primary, Chesi, Marta, primary, Bergsagel, P. Leif, primary, Bellone, Matteo, primary, Tonon, Giovanni, primary, Ciceri, Fabio, primary, Marcatti, Magda, primary, Caligaris-Cappio, Federico, primary, and Corti, Angelo, primary

Published
2023
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5. Supplementary Tables S1-S4 from Chromogranin A Is Preferentially Cleaved into Proangiogenic Peptides in the Bone Marrow of Multiple Myeloma Patients

Author

Bianco, Mimma, primary, Gasparri, Anna Maria, primary, Colombo, Barbara, primary, Curnis, Flavio, primary, Girlanda, Stefania, primary, Ponzoni, Maurilio, primary, Bertilaccio, Maria Teresa Sabrina, primary, Calcinotto, Arianna, primary, Sacchi, Angelina, primary, Ferrero, Elisabetta, primary, Ferrarini, Marina, primary, Chesi, Marta, primary, Bergsagel, P. Leif, primary, Bellone, Matteo, primary, Tonon, Giovanni, primary, Ciceri, Fabio, primary, Marcatti, Magda, primary, Caligaris-Cappio, Federico, primary, and Corti, Angelo, primary

Published
2023
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6. Supplementary Methods from Chromogranin A Is Preferentially Cleaved into Proangiogenic Peptides in the Bone Marrow of Multiple Myeloma Patients

Author

Bianco, Mimma, primary, Gasparri, Anna Maria, primary, Colombo, Barbara, primary, Curnis, Flavio, primary, Girlanda, Stefania, primary, Ponzoni, Maurilio, primary, Bertilaccio, Maria Teresa Sabrina, primary, Calcinotto, Arianna, primary, Sacchi, Angelina, primary, Ferrero, Elisabetta, primary, Ferrarini, Marina, primary, Chesi, Marta, primary, Bergsagel, P. Leif, primary, Bellone, Matteo, primary, Tonon, Giovanni, primary, Ciceri, Fabio, primary, Marcatti, Magda, primary, Caligaris-Cappio, Federico, primary, and Corti, Angelo, primary

Published
2023
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7. Myelomonocytic cells in giant cell arteritis activate trained immunity programs sustaining inflammation and cytokine production

Author

Cantoni, Eleonora, primary, Merelli, Ivan, additional, Stefanoni, Davide, additional, Tomelleri, Alessandro, additional, Campochiaro, Corrado, additional, Giordano, Vito, additional, Panigada, Maddalena, additional, Baldissera, Elena M, additional, Merlo Pich, Laura, additional, Natoli, Valentina, additional, Ziogas, Athanasios, additional, Domínguez-Andrés, Jorge, additional, De Luca, Giacomo, additional, Mazza, Davide, additional, Zambrano, Samuel, additional, Gnani, Daniela, additional, Ferrarini, Marina, additional, Ferrero, Elisabetta, additional, Agresti, Alessandra, additional, Vergani, Barbara, additional, Leone, Biagio Eugenio, additional, Cenci, Simone, additional, Ravelli, Angelo, additional, Matucci-Cerinic, Marco, additional, D’Alessandro, Angelo, additional, Joosten, Leo A B, additional, Dagna, Lorenzo, additional, Netea, Mihai G, additional, Molteni, Raffaella, additional, and Cavalli, Giulio, additional

Published
2023
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8. Myelomonocytic cells in giant cell arteritis activate trained immunity programs sustaining inflammation and cytokine production

Author

Cantoni, E, Merelli, I, Stefanoni, D, Tomelleri, A, Campochiaro, C, Giordano, V, Panigada, M, Baldissera, E, Merlo Pich, L, Natoli, V, Ziogas, A, Domínguez-Andrés, J, De Luca, G, Mazza, D, Zambrano, S, Gnani, D, Ferrarini, M, Ferrero, E, Agresti, A, Vergani, B, Leone, B, Cenci, S, Ravelli, A, Matucci-Cerinic, M, D'Alessandro, A, Joosten, L, Dagna, L, Netea, M, Molteni, R, Cavalli, G, Cantoni, Eleonora, Merelli, Ivan, Stefanoni, Davide, Tomelleri, Alessandro, Campochiaro, Corrado, Giordano, Vito, Panigada, Maddalena, Baldissera, Elena M, Merlo Pich, Laura, Natoli, Valentina, Ziogas, Athanasios, Domínguez-Andrés, Jorge, De Luca, Giacomo, Mazza, Davide, Zambrano, Samuel, Gnani, Daniela, Ferrarini, Marina, Ferrero, Elisabetta, Agresti, Alessandra, Vergani, Barbara, Leone, Biagio Eugenio, Cenci, Simone, Ravelli, Angelo, Matucci-Cerinic, Marco, D'Alessandro, Angelo, Joosten, Leo A B, Dagna, Lorenzo, Netea, Mihai G, Molteni, Raffaella, Cavalli, Giulio, Cantoni, E, Merelli, I, Stefanoni, D, Tomelleri, A, Campochiaro, C, Giordano, V, Panigada, M, Baldissera, E, Merlo Pich, L, Natoli, V, Ziogas, A, Domínguez-Andrés, J, De Luca, G, Mazza, D, Zambrano, S, Gnani, D, Ferrarini, M, Ferrero, E, Agresti, A, Vergani, B, Leone, B, Cenci, S, Ravelli, A, Matucci-Cerinic, M, D'Alessandro, A, Joosten, L, Dagna, L, Netea, M, Molteni, R, Cavalli, G, Cantoni, Eleonora, Merelli, Ivan, Stefanoni, Davide, Tomelleri, Alessandro, Campochiaro, Corrado, Giordano, Vito, Panigada, Maddalena, Baldissera, Elena M, Merlo Pich, Laura, Natoli, Valentina, Ziogas, Athanasios, Domínguez-Andrés, Jorge, De Luca, Giacomo, Mazza, Davide, Zambrano, Samuel, Gnani, Daniela, Ferrarini, Marina, Ferrero, Elisabetta, Agresti, Alessandra, Vergani, Barbara, Leone, Biagio Eugenio, Cenci, Simone, Ravelli, Angelo, Matucci-Cerinic, Marco, D'Alessandro, Angelo, Joosten, Leo A B, Dagna, Lorenzo, Netea, Mihai G, Molteni, Raffaella, and Cavalli, Giulio

Abstract

Objective: Trained immunity (TI) is a de facto memory program of innate immune cells, characterized by immunometabolic and epigenetic changes sustaining enhanced production of cytokines. TI evolved as a protective mechanism against infections; however, inappropriate activation can cause detrimental inflammation and might be implicated in the pathogenesis of chronic inflammatory diseases. In this study, we investigated the role of TI in the pathogenesis of giant cell arteritis (GCA), a large-vessel vasculitis characterized by aberrant macrophage activation and excess cytokine production. Methods: Monocytes from GCA patients and from age- and sex-matched healthy donors were subjected to polyfunctional studies, including cytokine production assays at baseline and following stimulation, intracellular metabolomics, chromatin immunoprecipitation-qPCR, and combined ATAC/RNA sequencing. Immunometabolic activation (i.e. glycolysis) was assessed in inflamed vessels of GCA patients with FDG-PET and immunohistochemistry (IHC), and the role of this pathway in sustaining cytokine production was confirmed with selective pharmacologic inhibition in GCA monocytes. Results: GCA monocytes exhibited hallmark molecular features of TI. Specifically, these included enhanced IL-6 production upon stimulation, typical immunometabolic changes (e.g. increased glycolysis and glutaminolysis) and epigenetic changes promoting enhanced transcription of genes governing pro-inflammatory activation. Immunometabolic changes of TI (i.e. glycolysis) were a feature of myelomonocytic cells in GCA lesions and were required for enhanced cytokine production. Conclusions: Myelomonocytic cells in GCA activate TI programs sustaining enhanced inflammatory activation with excess cytokine production.

Published
2023

11. Immunometabolic activation of macrophages leads to cytokine production in the pathogenesis of KRAS-mutated histiocytosis

Author

Ferrero, Elisabetta, primary, Villa, Antonello, additional, Stefanoni, Davide, additional, Nemkov, Travis, additional, D’Alessandro, Angelo, additional, Tengesdal, Isak, additional, Belloni, Daniela, additional, Molteni, Raffaella, additional, Vergani, Barbara, additional, De Luca, Giacomo, additional, Grassini, Greta, additional, Cangi, Maria Giulia, additional, Dagna, Lorenzo, additional, Doglioni, Claudio, additional, Cavalli, Giulio, additional, and Ferrarini, Marina, additional

Published
2021
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12. Immunometabolic activation of macrophages leads to cytokine production in the pathogenesis of KRAS-mutated histiocytosis.

Author

Ferrero, Elisabetta, Villa, Antonello, Stefanoni, Davide, Nemkov, Travis, D'Alessandro, Angelo, Tengesdal, Isak, Belloni, Daniela, Molteni, Raffaella, Vergani, Barbara, Luca, Giacomo De, Grassini, Greta, Cangi, Maria Giulia, Dagna, Lorenzo, Doglioni, Claudio, Cavalli, Giulio, and Ferrarini, Marina

Subjects
CYTOKINES, GENETIC mutation, SKIN, PROTEIN kinase inhibitors, IMMUNOHISTOCHEMISTRY, MACROPHAGES, LANGERHANS-cell histiocytosis, GENE expression, CELLULAR signal transduction, CYTOKINE release syndrome, PHOSPHORYLATION
Abstract

The article presents a case study which characterized the functional and metabolic outcomes of an activating Kirsten rat sarcoma viral oncogene homologue (KRAS) mutation in a patient affected by Langerhans-related histiocytosis. Topics include case of a patient with articular, pituitary and skin involvement, comparison between the supernatant of tissue lesions and tissue culture medium, and clinical effectiveness MAPK pathway inhibition with selective MEK inhibitors in histiocytosis patients.

Published
2022
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13. Oncogene-induced maladaptive activation of trained immunity in the pathogenesis and treatment of Erdheim-Chester disease

Author

Molteni, Raffaella, Biavasco, Riccardo, Stefanoni, Davide, Nemkov, Travis, Domínguez-Andrés, Jorge, Arts, Rob J., Merelli, Ivan, Mazza, Davide, Zambrano, Samuel, Panigada, Maddalena, Cantoni, Eleonora, Tengesdal, Isak W., Maksud, Philippe, Piras, Francesco, Cesana, Daniela, Cassina, Laura, Distefano, Gianfranco, Loffreda, Alessia, Gnani, Daniela, De Luca, Giacomo, Tomelleri, Alessandro, Campochiaro, Corrado, Joosten, Leo A.B., Dinarello, Charles A., Kajaste-Rudnitski, Anna, Haroche, Julien, Cardaci, Simone, Cenci, Simone, Dagna, Lorenzo, Doglioni, Claudio, Ferrarini, Marina, Ferrero, Elisabetta, Boletta, Alessandra, D'Alessandro, Angelo, Montini, Eugenio, Netea, Mihai G., and Cavalli, Giulio

Abstract

Trained immunity (TI) is a proinflammatory program induced in monocyte/macrophages upon sensing of specific pathogens and is characterized by immunometabolic and epigenetic changes that enhance cytokine production. Maladaptive activation of TI (ie, in the absence of infection) may result in detrimental inflammation and development of disease; however, the exact role and extent of inappropriate activation of TI in the pathogenesis of human diseases is undetermined. In this study, we uncovered the oncogene-induced, maladaptive induction of TI in the pathogenesis of a human inflammatory myeloid neoplasm (Erdheim-Chester disease, [ECD]), characterized by the BRAFV600E oncogenic mutation in monocyte/macrophages and excess cytokine production. Mechanistically, myeloid cells expressing BRAFV600E exhibit all molecular features of TI: activation of the AKT/mammalian target of rapamycin signaling axis; increased glycolysis, glutaminolysis, and cholesterol synthesis; epigenetic changes on promoters of genes encoding cytokines; and enhanced cytokine production leading to hyperinflammatory responses. In patients with ECD, effective therapeutic strategies combat this maladaptive TI phenotype; in addition, pharmacologic inhibition of immunometabolic changes underlying TI (ie, glycolysis) effectively dampens cytokine production by myeloid cells. This study revealed the deleterious potential of inappropriate activation of TI in the pathogenesis of human inflammatory myeloid neoplasms and the opportunity for inhibition of TI in conditions characterized by maladaptive myeloid-driven inflammation.

Published
2021
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14. Immunometabolic activation of macrophages leads to cytokine production in the pathogenesis of KRAS-mutated histiocytosis

Author

Elisabetta Ferrero, Antonello Villa, Davide Stefanoni, Travis Nemkov, Angelo D’Alessandro, Isak Tengesdal, Daniela Belloni, Raffaella Molteni, Barbara Vergani, Giacomo De Luca, Greta Grassini, Maria Giulia Cangi, Lorenzo Dagna, Claudio Doglioni, Giulio Cavalli, Marina Ferrarini, Ferrero, Elisabetta, Villa, Antonello, Stefanoni, Davide, Nemkov, Travi, D'Alessandro, Angelo, Tengesdal, Isak, Belloni, Daniela, Molteni, Raffaella, Vergani, Barbara, De Luca, Giacomo, Grassini, Greta, Cangi, Maria Giulia, Dagna, Lorenzo, Doglioni, Claudio, Cavalli, Giulio, Ferrarini, Marina, Ferrero, E, Villa, A, Stefanoni, D, Nemkov, T, D'Alessandro, A, Tengesdal, I, Belloni, D, Molteni, R, Vergani, B, De Luca, G, Grassini, G, Giulia Cangi, M, Dagna, L, Doglioni, C, Cavalli, G, and Ferrarini, M

Subjects
Proto-Oncogene Proteins p21(ras), Rheumatology, 3D culture, histiocytosis tissue, KRAS, immunometabolism, macrophage activation, Macrophages, Mutation, MED/06 - ONCOLOGIA MEDICA, Cytokines, Gene Expression, Humans, Pharmacology (medical), Histiocytosis
Published
2021

15. 3D Models of Surrogate Multiple Myeloma Bone Marrow Microenvironments : Insights on Disease Pathophysiology and Patient-Specific Response to Drugs

Author

Ferrero, Elisabetta and Ferrarini, Marina

Subjects
Medical
Abstract

Multiple Myeloma (MM) develops almost exclusively within the Bone Marrow (BM), highlighting the critical role of the microenvironment in conditioning disease progression and resistance to drugs. Indeed, while the therapeutic armamentarium for MM has significantly improved over the past 20 years, the disease remains ultimately incurable. This failure may depend on the high phenotypic and genetic heterogeneity of MM, but also on the paucity and inadequacy of two-dimensional (2D) conventional preclinical models in reproducing MM within the BM. In the present paper, we provide a brief updated overview on MM BM microenvironment. We then discuss newly developed preclinical models mimicking MM/microenvironment interactions, including three-dimensional (3D), gel-based, in vitro models and a novel ex vivo system of isolated tumor and stromal cells cultured in bioreactor. Potential applications of each model, relative to investigation of MM pathogenic mechanisms and prediction of the best drug/combination for each individual patient will be also evaluated.

Published
2022

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