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Your search keyword '"Maurizio Miglino"' showing total 16 results
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16 results on '"Maurizio Miglino"'

1. Clonal hematopoiesis impacts frailty in newly diagnosed multiple myeloma patients: a retrospective multicenter analysis

Author

Elisa Gelli, Claudia Martinuzzi, Debora Soncini, Concetta Conticello, Francesco Ladisa, Giulia Giorgetti, Dario Truffelli, Isabella Traverso, Francesco Lai, Fabio Guolo, Maurizio Miglino, Antonia Cagnetta, Antonella Laudisi, Sara Aquino, Daniele Derudas, Francesco Di Raimondo, Domenico A. Coviello, Roberto M. Lemoli, and Michele Cea

Subjects
Multiple myeloma, Biomarkers, CHIP, Toxicity, Frailty, Medicine, Science
Abstract

Abstract Somatic mutations of hematopoietic cells in the peripheral blood of normal individuals refer to clonal hematopoiesis of indeterminate potential (CHIP), which is associated with a 0.5–1% risk of progression to hematological malignancies and cardiovascular diseases. CHIP has also been reported in Multiple Myeloma (MM) patients, but its biological relevance remains to be elucidated. In this study, high-depth targeted sequencing of peripheral blood from 76 NDMM patients revealed CHIP in 46% of them, with a variant allele frequency (VAF) ranging from ~ 1 to 34%. The most frequently mutated gene was DNMT3A, followed by TET2. More aggressive disease features were observed among CHIP carriers, who also exhibited higher proportion of high-risk stages (ISS and R-ISS 3) compared to controls. Longitudinal analyses at diagnosis and during follow-up showed a slight increase of VAFs (p = 0.058) for epigenetic (DNMT3A, TET2, and ASXL1) and DNA repair genes (TP53; p = 0.0123). A more stable frequency was observed among other genes, suggesting different temporal dynamics of CH clones. Adverse clinical outcomes, in term of overall and progression-free survivals, were observed in CHIP carriers. These patients also exhibited weakened immune T-cells and enhanced frailty, predicting greater toxicity and consequently shorter event-free survival. Finally, correlation analysis identified platelets count as biomarker for higher VAF among CHIP carriers, regardless of the specific variant. Overall, our study highlights specific biological and clinical features, paving the way for the development of tailored strategies for MM patients carrying CHIP.

Published
2024
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2. Determinants of Covid19 disease and of survival after Covid19 in MPN patients treated with ruxolitinib

Author

Francesca Palandri, Elena M. Elli, Giuseppe Auteri, Massimiliano Bonifacio, Giulia Benevolo, Florian H. Heidel, Simona Paglia, Malgorzata M. Trawinska, Costanza Bosi, Elena Rossi, Mario Tiribelli, Alessia Tieghi, Alessandra Iurlo, Nicola Polverelli, Giovanni Caocci, Gianni Binotto, Francesco Cavazzini, Eloise Beggiato, Daniela Cilloni, Caterina Tatarelli, Francesco Mendicino, Maurizio Miglino, Monica Bocchia, Monica Crugnola, Camilla Mazzoni, Andrea D. Romagnoli, Giovanni Rindone, Sara Ceglie, Alessandra D’Addio, Eleonora Santoni, Daniele Cattaneo, Daniela Bartoletti, Roberto M. Lemoli, Mauro Krampera, Antonio Cuneo, Gianpietro C. Semenzato, Roberto Latagliata, Elisabetta Abruzzese, Nicola Vianelli, Michele Cavo, Alessandro Andriani, Valerio De Stefano, Giuseppe A. Palumbo, and Massimo Breccia

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Published
2023
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3. S217: POST-TRANSPLANT NIVOLUMAB PLUS UNSELECTED AUTOLOGOUS LYMPHOCYTES IN REFRACTORY HODGKIN LYMPHOMA RESULTS IN VERY HIGH REMISSION RATE AND EXCELLENT SURVIVAL AND IT IS ASSOCIATED WITH NK CELL EXPANSION

Author

Fabio Guolo, Paola Minetto, Silvia Pesce, Filippo Ballerini, Michele Cea, Marco Greppi, Matteo Bozzo, Maurizio Miglino, Elisabetta Tedone, Alessandra Bo, Alberto Serio, Silvia Luchetti, Simona Candiani, Marco Mora, Vanessa Agostini, Paolo Nozza, Genny Del Zotto, Emanuela Marcenaro, and Roberto Massimo Lemoli

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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4. P381: FULL PEDIATRIC INDUCTION IN ADULTS AGED UP TO 55 YEARS WITH PHILADELPHIA-NEGATIVE ACUTE LYMPHOBLASTIC LEUKEMIA IS WELL TOLERATED AND RESULTS IN VERY HIGH CURE RATE

Author

Elena Maio, Mattia Montanari, Francesco Puglisi, Clara Nurra, Maurizio Miglino, Nicoletta Colombo, Enrico Carminati, Giada Zecchetti, Chiara Vernarecci, Maria Chies, Beatrice Ferro, Massimo Zucchetti, Antonia Cagnetta, Michele Cea, Elisabetta Tedone, Roberto Massimo Lemoli, Fabio Guolo, and Paola Minetto

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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5. P530: CPX-351 INDUCTION IS ABLE TO INDUCE MRD NEGATIVE CR IN A SIGNIFICATIVE PROPORTION OF VERY HIGH RISK AML PATIENTS, REGARDLESS OF MUTATIONAL BURDEN, ALLOWING FOR BRIDGING TO TRANSPLANTATION

Author

Carola Riva, Maria Chies, Paola Minetto, Chiara Vernarecci, Elena Maio, Beatrice Ferro, Giada Zecchetti, Maurizio Miglino, Elisabetta Tedone, Nicoletta Colombo, Enrico Carminati, Clara Nurra, Francesco Puglisi, Antonia Cagnetta, Michele Cea, Roberto Massimo Lemoli, and Fabio Guolo

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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6. P1028: MYELOFIBROSIS (MF) TREATED WITH RUXOLITINIB (RUX) MONOTHERAPY: PREDICTORS OF EARLY DISCONTINUATION AND DEATH ON TREATMENT. THE SHORT-TERM RUX PROGNOSTIC MODEL (STR-PM)

Author

Francesca Palandri, Giuseppe Auteri, Alessandra Iurlo, Elena Maria Elli, Simona Paglia, Massimiliano Bonifacio, Mario Tiribelli, Malgorzata Monica Trawinska, Nicola Polverelli, Giulia Benevolo, Alessia Tieghi, Florian Heidel, Fabrizio Cavalca, Giovanni Caocci, Eloise Beggiato, Gianni Binotto, Francesco Cavazzini, Maurizio Miglino, Costanza Bosi, Monica Crugnola, Monica Bocchia, Bruno Martino, Novella Pugliese, Marta Venturi, Camilla Mazzoni, Alessandro Isidori, Daniele Cattaneo, Mauro Krampera, Fabrizio Pane, Daniela Cilloni, Gianpietro Semenzato, Roberto M. Lemoni, Antonio Cuneo, Elisabetta Abruzzese, Nicola Vianelli, Michele Cavo, Giuseppe Palumbo, and Massimo Breccia

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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7. PB1742: FEASIBILITY AND EFFICACY OF A PEG-ASPARAGINASE-BASED TREATMENT PROTOCOL IN ELDERLY PHILADELPHIA-NEGATIVE ACUTE LYMPHOBLASTIC LEUKEMIA PATIENTS

Author

Chiara Vernarecci, Beatrice Ferro, Francesco Puglisi, Clara Nurra, Enrico Carminati, Carola Riva, Maria Chies, Elena Maio, Giada Zecchetti, Maurizio Miglino, Nicoletta Colombo, Filippo Ballerini, Antonia Cagnetta, Michele Cea, Elisabetta Tedone, Fabio Guolo, Paola Minetto, and Roberto Massimo Lemoli

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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8. CD38-Induced Metabolic Dysfunction Primes Multiple Myeloma Cells for NAD+-Lowering Agents

Author

Pamela Becherini, Debora Soncini, Silvia Ravera, Elisa Gelli, Claudia Martinuzzi, Giulia Giorgetti, Antonia Cagnetta, Fabio Guolo, Federico Ivaldi, Maurizio Miglino, Sara Aquino, Katia Todoerti, Antonino Neri, Andrea Benzi, Mario Passalacqua, Alessio Nencioni, Ida Perrotta, Maria Eugenia Gallo Cantafio, Nicola Amodio, Antonio De Flora, Santina Bruzzone, Roberto M. Lemoli, and Michele Cea

Subjects
NAD+ biosynthetic pathway, NAD+-lowering agents, cancer metabolism, mitochondrial disfunction, oxidative stress, multiple myeloma, Therapeutics. Pharmacology, RM1-950
Abstract

Cancer cells fuel growth and energy demands by increasing their NAD+ biosynthesis dependency, which therefore represents an exploitable vulnerability for anti-cancer strategies. CD38 is a NAD+-degrading enzyme that has become crucial for anti-MM therapies since anti-CD38 monoclonal antibodies represent the backbone for treatment of newly diagnosed and relapsed multiple myeloma patients. Nevertheless, further steps are needed to enable a full exploitation of these strategies, including deeper insights of the mechanisms by which CD38 promotes tumorigenesis and its metabolic additions that could be selectively targeted by therapeutic strategies. Here, we present evidence that CD38 upregulation produces a pervasive intracellular-NAD+ depletion, which impairs mitochondrial fitness and enhances oxidative stress; as result, genetic or pharmacologic approaches that aim to modify CD38 surface-level prime MM cells to NAD+-lowering agents. The molecular mechanism underlying this event is an alteration in mitochondrial dynamics, which decreases mitochondria efficiency and triggers energetic remodeling. Overall, we found that CD38 handling represents an innovative strategy to improve the outcomes of NAD+-lowering agents and provides the rationale for testing these very promising agents in clinical studies involving MM patients.

Published
2023
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9. Ruxolitinib in cytopenic myelofibrosis: Response, toxicity, drug discontinuation, and outcome

Author

Francesca Palandri, Massimo Breccia, Camilla Mazzoni, Giuseppe Auteri, Elena Maria Elli, Malgorzata M. Trawinska, Nicola Polverelli, Mario Tiribelli, Giulia Benevolo, Alessandra Iurlo, Alessia Tieghi, Florian H. Heidel, Giovanni Caocci, Eloise Beggiato, Gianni Binotto, Francesco Cavazzini, Maurizio Miglino, Costanza Bosi, Monica Crugnola, Monica Bocchia, Bruno Martino, Novella Pugliese, Mattia Biondo, Marta Venturi, Luigi Scaffidi, Alessandro Isidori, Daniele Cattaneo, Mauro Krampera, Fabrizio Pane, Daniela Cilloni, Gianpietro Semenzato, Roberto M. Lemoli, Antonio Cuneo, Elisabetta Abruzzese, Daniela Bartoletti, Simona Paglia, Nicola Vianelli, Michele Cavo, Massimiliano Bonifacio, and Giuseppe A. Palumbo

Subjects
Cancer Research, Oncology, ruxolitinib, cytopenia, myelofibrosis, myelodepletive phenotype, myeloproliferative neoplasms
Published
2023
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10. Treatment-Free Remission Outcome in Patients with Chronic Myeloid Leukemia in Chronic Phase Following One Year of Nilotinib De-Escalation: 96-Week Update of Dante Study

Author

Fabio Stagno, Elisabetta Abruzzese, Alessandra Iurlo, Fabrizio Pane, Imma Attolico, Paolo Sportoletti, Patrizia Pregno, Sara Galimberti, Barbara Scappini, Maurizio Miglino, Sergio Siragusa, Isabella Capodanno, Diletta Valsecchi, Aurelio Pio Nardozza, Paola Coco, Gianantonio Rosti, Giuseppe Saglio, and Massimo Breccia

Subjects
Immunology, Cell Biology, Hematology, Biochemistry
Published
2022
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11. Real-World Management of Advanced Systemic Mastocytosis Treated with Midostaurin: Analysis of Patients Who Completed 12 Months of Follow-up from an Italian Observational Study (OVIDIO)

Author

Cristina Papayannidis, Francesco Mannelli, Lara Crosera, Roberta Parente, Alessandra Romano, Michela Rondoni, Chiara Elena, Marianna Criscuolo, Nicola Di Renzo, Fiorina Giona, Fabrizio Pane, Daniela Cilloni, Elena Maria Elli, Maurizio Miglino, Patrizio Mazza, Alessandra Malato, Lara Pochintesta, Roberta Bini, Diletta Valsecchi, and Federica Irene Grifoni

Subjects
Immunology, Cell Biology, Hematology, Biochemistry
Published
2022
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12. Suppl. Figures 1-10 from Dual NAMPT and BTK Targeting Leads to Synergistic Killing of Waldenström Macroglobulinemia Cells Regardless of MYD88 and CXCR4 Somatic Mutation Status

Author

Kenneth C. Anderson, Steven P. Treon, Nikhil Munshi, Roberto M. Lemoli, Marco Gobbi, Dharminder Chauhan, Teru Hideshima, Alberto Ballestrero, Fiammetta Monacelli, Fabrizio Montecucco, Alessio Nencioni, Luca Mastracci, Giulio Fraternali-Orcioni, Maurizio Miglino, Debora Soncini, Davide Lovera, Cao Yang, Yu-Tzu Tai, Prakrati Acharya, Chirag Acharya, Antonia Cagnetta, and Michele Cea

Abstract

Suppl. Fig.1. Nampt staining on normal Lymph Nodes; Suppl. Fig. 2. Nampt over-expression in BCMW.1 cells. Suppl. Fig. 3. Dose-response effect curves of FK866; Suppl. Fig. 4. Expression levels of Nampt in WM cells after BTK inhibition (GSE65816); Suppl. Fig. 5. MYD88 L265P and MYD88 WT expressing cells treated with FK866, ibrutinib, or both. Suppl. Fig. 6. MYD88 L265P (BCMW.1 and MWCL-1) and MYD88 WT ( MEC.1 and RL) expressing cells were treated with an inhibitor of Nampt (FK866), BTK (ibrutinib), or both. Suppl. Fig. 7. Effects of co-treatment on primary tumor cells. Suppl. Fig. 8. Densitometric analysis of WB represented in Figure 3B. Suppl. Fig. 9. Rescue experiments with exogenous NAD. Suppl. Fig. 10. Effects of co-treatments on animals body weight.

Published
2023
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13. Suppl. Figures legends from Dual NAMPT and BTK Targeting Leads to Synergistic Killing of Waldenström Macroglobulinemia Cells Regardless of MYD88 and CXCR4 Somatic Mutation Status

Author

Kenneth C. Anderson, Steven P. Treon, Nikhil Munshi, Roberto M. Lemoli, Marco Gobbi, Dharminder Chauhan, Teru Hideshima, Alberto Ballestrero, Fiammetta Monacelli, Fabrizio Montecucco, Alessio Nencioni, Luca Mastracci, Giulio Fraternali-Orcioni, Maurizio Miglino, Debora Soncini, Davide Lovera, Cao Yang, Yu-Tzu Tai, Prakrati Acharya, Chirag Acharya, Antonia Cagnetta, and Michele Cea

Abstract

Suppl. figure legends

Published
2023
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14. Data from Dual NAMPT and BTK Targeting Leads to Synergistic Killing of Waldenström Macroglobulinemia Cells Regardless of MYD88 and CXCR4 Somatic Mutation Status

Author

Kenneth C. Anderson, Steven P. Treon, Nikhil Munshi, Roberto M. Lemoli, Marco Gobbi, Dharminder Chauhan, Teru Hideshima, Alberto Ballestrero, Fiammetta Monacelli, Fabrizio Montecucco, Alessio Nencioni, Luca Mastracci, Giulio Fraternali-Orcioni, Maurizio Miglino, Debora Soncini, Davide Lovera, Cao Yang, Yu-Tzu Tai, Prakrati Acharya, Chirag Acharya, Antonia Cagnetta, and Michele Cea

Abstract

Purpose: Nicotinamide phosphoribosyltransferase (Nampt) regulates intracellular NAD+ pool and is highly expressed in a number of malignancies. FK866, a selective inhibitor of Nampt, depletes intracellular NAD+ levels, thereby blocking cellular metabolism and triggering sensitization to other drugs and cell death. Here we characterized the antitumor effects of Nampt inhibition in Waldenström macroglobulinemia.Experimental Design: We investigated Nampt role in MW cells using both mRNA and protein expression analyses. We have also used loss-of-function approaches to investigate the growth and survival effects of Nampt on MW cells and further tested the anti-MW activity of dual Nampt and BTK inhibition in vitro and in vivo.Results: We found that Waldenström macroglobulinemia cells exhibit high levels of Nampt compared with normal B cells. Loss of function studies suggested a potential oncogenic role of Nampt in Waldenström macroglobulinemia cells, and BTK-inhibitor ibrutinib and FK866 resulted in a significant and synergistic anti-Waldenström macroglobulinemia cell death, regardless of MYD88 and CXCR4 mutational status. Cell death was associated with: (i) activation of caspase-3, PARP and downregulation of Mcl-1, (ii) enhanced intracellular ATP and NAD+ depletion, (iii) inhibition of NF-κB signaling, and (iv) inhibition of multiple prosurvival signaling pathways. In a murine xenograft Waldenström macroglobulinemia model, low-dose combination FK866 and ibrutinib is well tolerated, significantly inhibits tumor growth, and prolongs host survival.Conclusions: Our results show intracellular NAD+ level as crucial for proliferation and survival of Waldenström macroglobulinemia cells, and provides the mechanistic preclinical rationale for targeting Nampt, either alone or with Ibrutinib, to overcome drug resistance and improve patient outcome in Waldenström macroglobulinemia. Clin Cancer Res; 22(24); 6099–109. ©2016 AACR.

Published
2023
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16. Prognostic Relevance of Minimal Residual Disease in Therapy Related and Secondary Acute Myeloid Leukemia Receiving CPX-351 or Fludarabine-Based Induction

Author

Fabio Guolo, Paola Minetto, Carola Riva, Chiara Vernarecci, Monica Passannante, Francesca Parodi, Michela Frello, Elena Maio, Beatrice Ferro, Maria Chies, Maurizio Miglino, Elisabetta Tedone, Nicoletta Colombo, Enrico Carminati, Clara Nurra, Francesco Puglisi, Antonia Cagnetta, Michele Cea, and Roberto Massimo Lemoli

Subjects
Immunology, Cell Biology, Hematology, Biochemistry
Published
2022
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