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11 results on '"Lunghi, Monia"'

1. AVALON: The Italian cohort study on real-life efficacy of hypomethylating agents plus venetoclax in newly diagnosed or relapsed/refractory patients with acute myeloid leukemia

Author

Todisco, Elisabetta, Papayannidis, Cristina, Fracchiolla, Nicola, Petracci, Elisabetta, Zingaretti, Chiara, Vetro, Calogero, Martelli, Maria Paola, Zappasodi, Patrizia, Di Renzo, Nicola, Gallo, Susanna, Audisio, Ernesta, Griguolo, Davide, Cerchione, Claudio, Selleri, Carmine, Mattei, Daniele, Bernardi, Massimo, Fumagalli, Monica, Rizzuto, Giuliana, Facchini, Luca, Basilico, Claudia Maria, Manfra, Ilenia, Borlenghi, Erika, Cairoli, Roberto, Salutari, Prassede, Gottardi, Michele, Molteni, Alfredo, Martini, Vincenza, Lunghi, Monia, Fianchi, Luana, Cilloni, Daniela, Lanza, Francesco, Abruzzese, Elisabetta, Cascavilla, Nicola, Rivellini, Flavia, Ferrara, Felicetto, Maurillo, Luca, Nanni, Jacopo, Romano, Alessandra, Cardinali, Valeria, Gigli, Federica, Roncoroni, Elisa, Federico, Vincenzo, Marconi, Giovanni, Volpi, Roberta, Sciumè, Mariarita, Tarella, Corrado, Rossi, Giuseppe, Martinelli, Giovanni, Todisco, Elisabetta, Papayannidis, Cristina, Fracchiolla, Nicola, Petracci, Elisabetta, Zingaretti, Chiara, Vetro, Calogero, Martelli, Maria Paola, Zappasodi, Patrizia, Di Renzo, Nicola, Gallo, Susanna, Audisio, Ernesta, Griguolo, Davide, Cerchione, Claudio, Selleri, Carmine, Mattei, Daniele, Bernardi, Massimo, Fumagalli, Monica, Rizzuto, Giuliana, Facchini, Luca, Basilico, Claudia Maria, Manfra, Ilenia, Borlenghi, Erika, Cairoli, Roberto, Salutari, Prassede, Gottardi, Michele, Molteni, Alfredo, Martini, Vincenza, Lunghi, Monia, Fianchi, Luana, Cilloni, Daniela, Lanza, Francesco, Abruzzese, Elisabetta, Cascavilla, Nicola, Rivellini, Flavia, Ferrara, Felicetto, Maurillo, Luca, Nanni, Jacopo, Romano, Alessandra, Cardinali, Valeria, Gigli, Federica, Roncoroni, Elisa, Federico, Vincenzo, Marconi, Giovanni, Volpi, Roberta, Sciumè, Mariarita, Tarella, Corrado, Rossi, Giuseppe, Martinelli, Giovanni, Todisco, E, Papayannidis, C, Fracchiolla, N, Petracci, E, Zingaretti, C, Vetro, C, Martelli, M, Zappasodi, P, Di Renzo, N, Gallo, S, Audisio, E, Griguolo, D, Cerchione, C, Selleri, C, Mattei, D, Bernardi, M, Fumagalli, M, Rizzuto, G, Facchini, L, Basilico, C, Manfra, I, Borlenghi, E, Cairoli, R, Salutari, P, Gottardi, M, Molteni, A, Martini, V, Lunghi, M, Fianchi, L, Cilloni, D, Lanza, F, Abruzzese, E, Cascavilla, N, Rivellini, F, Ferrara, F, Maurillo, L, Nanni, J, Romano, A, Cardinali, V, Gigli, F, Roncoroni, E, Federico, V, Marconi, G, Volpi, R, Sciumè, M, Tarella, C, Rossi, G, and Martinelli, G

Subjects
Cancer Research, hypomethylating agents, Oncology, hypomethylating agent, relapsed and refractory AML, venetoclax, real-life data, acute myeloid leukemia
Abstract

Background: Venetoclax in combination with hypomethylating agents (HMA) is revolutionizing the therapy of acute myeloid leukemia (AML). However, evidence on large sets of patients is lacking, especially in relapsed or refractory leukemia. Methods: AVALON is a multicentric cohort study that was conducted in Italy on patients with AML who received venetoclax-based therapies from 2015 to 2020. The study was approved by the ethics committee of the participating institution and was conducted in accordance with the Declaration of Helsinki. The effectiveness and toxicity of venetoclax+HMA in 190 (43 newly diagnosed, 68 refractory, and 79 relapsed) patients with AML are reported here. Results: In the newly diagnosed AML, the overall response rate and survival confirmed the brilliant results demonstrated in VIALE-A. In the relapsed or refractory AML, the combination demonstrated a surprisingly complete remission rate (44.1% in refractory and 39.7% in relapsed evaluable patients) and conferred to treated patients a good expectation of survival. Toxicities were overall manageable, and most incidents occurred in the first 60days of therapy. Infections were confirmed as the most common nonhematologic adverse event. Conclusions: Real-life data show that the combination of venetoclax and HMA offers an expectation of remission and long-term survival to elderly, newly diagnosed patients, and to relapsed or chemoresistant AML, increasing the chance of cure through a different mechanism of action. The venetoclax+HMA combination is expected to constitute the base for triplet combinations and integration of target therapies. Our data contribute to ameliorate the understanding of venetoclax+HMA effectiveness and toxicities in real life.

Published
2023

2. Molecular response and Quality of Life (QoL) in Chronic Myeloid Leukemia (CML) patients treated with Intermittent TKIs: first interim analysis of OPTkIMA Study

Author

Michele Malagola, Iurlo, Alessandra, Abruzzese, Elisabetta, Bonifacio, Massimiliano, Stagno, Fabio, Binotto, Gianni, D’adda, Mariella, Lunghi, Monia, Crugnola, Monica, Ferrari Maria Luisa, Lunghi, Francesca, Castagnetti, Fausto, Rosti, Gianantonio, Lemoli Roberto Massimo, Sancetta, Rosaria, Coppi Maria Rosaria, Corsetti Maria Teresa, Rege Cambrin Giovanna, Romano, Atelda, Tiribelli, Mario, Russo Rossi Antonella, Russo, Sabina, Aprile, Lara, Gandolfi, Lisa, Mirko Farina, Simona Bernardi, Polverelli, Nicola, Roccaro, Aldo Maria, De Vivo Antonio, Baccarani, Michele, and Russo, Domenico

Published
2021

3. A Retrospective Real-Life Report on Newly Diagnosed Adult Ph plus Acute Lymphoblastic Leukemia (Ph plus ALL) Patients Treated in Italy - The CAMPUS-ALL Experience

Author

Dragani, Matteo, Agrippino, Roberta, Cambrin, Giovanna Rege, Mancini, Valentina, Annunziata, Mario, Lunghi, Monia, Ciccone, Maria, Malato, Alessandra, Patrizia Chiusolo, Fava, Carmen, Berchialla, Paola, Foa, Roberto, and Chiaretti, Sabina

Subjects
real life, acute lymphoblastic leukemia, ALL, Philadelphia-positive leukemia, TKI
Published
2020

4. Rotation of nilotinib and imatinib for first-line treatment of chronic phase chronic myeloid leukemia

Author

Gugliotta, Gabriele, Castagnetti, Fausto, Breccia, Massimo, Gozzini, Antonella, Usala, Emilio, Carella, Angelo M., Rege cambrin, Giovanna, Martino, Bruno, Abruzzese, Elisabetta, Albano, Francesco, Stagno, Fabio, Luciano, Luigia, D'Adda, Mariella, Bocchia, Monica, Cavazzini, Francesco, Tiribelli, Mario, Lunghi, Monia, Pia Falcone, Antonietta, Musolino, Caterina, Levato, Luciano, Venturi, Claudia, Soverini, Simona, Cavo, Michele, Alimena, Giuliana, Pane, Fabrizio, Martinelli, Giovanni, Saglio, Giuseppe, Rosti, Gianantonio, Baccarani, Michele, Gugliotta, Gabriele, Castagnetti, Fausto, Breccia, Massimo, Gozzini, Antonella, Usala, Emilio, Carella, Angelo M., Rege Cambrin, Giovanna, Martino, Bruno, Abruzzese, Elisabetta, Albano, Francesco, Stagno, Fabio, Luciano, Luigia, D'Adda, Mariella, Bocchia, Monica, Cavazzini, Francesco, Tiribelli, Mario, Lunghi, Monia, Pia Falcone, Antonietta, Musolino, Caterina, Levato, Luciano, Venturi, Claudia, Soverini, Simona, Cavo, Michele, Alimena, Giuliana, Pane, Fabrizio, Martinelli, Giovanni, Saglio, Giuseppe, Rosti, Gianantonio, Baccarani, Michele, and Rege-Cambrin, Giovanna

Subjects
Myeloid, Adult, Male, Adolescent, Aged, Aged, 80 and over, Cardiovascular Diseases, Drug Administration Schedule, Female, Humans, Imatinib Mesylate, Leukemia, Myeloid, Chronic-Phase, Middle Aged, Protein Kinase Inhibitors, Pyrimidines, Survival Analysis, Survival Rate, Treatment Outcome, Young Adult, Hematology, Socio-culturale, hemic and lymphatic diseases, 80 and over, Leukemia, Medicine (all), Hematology, nilotimib, chronic myeloid leukemia, respiratory tract diseases, Chronic-Phase
Abstract

The introduction of second-generation tyrosine-kinase inhibitors (TKIs) has generated a lively debate on the choice of first-line TKI in chronic phase, chronic myeloid leukemia (CML). Despite the TKIs have different efficacy and toxicity profiles, the planned use of two TKIs has never been investigated. We report on a phase 2 study that was designed to evaluate efficacy and safety of a treatment alternating nilotinib and imatinib, in newly diagnosed BCR-ABL1 positive, chronic phase, CML patients. One hundred twenty-three patients were enrolled. Median age was 56 years. The probabilities of achieving a complete cytogenetic response, a major molecular response, and a deep molecular response (MR 4.0) by 2 years were 93%, 87%, and 61%, respectively. The 5-year overall survival and progression-free survival were 89%. Response rates and survival are in the range of those reported with nilotinib alone. Moreover, we observed a relatively low rate of cardiovascular adverse events (5%). These data show that the different efficacy and toxicity profiles of TKIs could be favorably exploited by alternating their use. Am. J. Hematol. 91:617-622, 2016. © 2016 Wiley Periodicals, Inc.

Published
2016

5. Myelodysplastic syndromes with single neutropenia or thrombocytopenia are rarely refractory cytopenias with unilineage dysplasia by World Health Organization 2008 criteria and have favourable prognosis

Author

Beyne-Rauzy, Odile, Sebert, Marie, Sapena, Rosa, Zerazhi, Hacène, Legros, Laurence, Guerci-Bresler, Agnès, Ame, Shanti Natarjan, Germing, Ulrich, Santini, Valeria, Salvi, Flavia, Gioia, Daniela, Lunghi, Monia, Dreyfus, François, Fenaux, Pierre, Sindromi, Fdn Italiana, Registry, Dusseldorf Mds, Gyan, Emmanuel, Andrieu, Valerie, Sanna, Alessandro, Caille, Agnès, Schemenau, Jennifer, Sudaka, Isabelle, Siguret, Virginie, Malet, Michele, Park, Sophie, Bordessoule, Dominique, Mairesse, Jacques, Gelsi-Boyer, Véronique, Cheze, Stephane, Service Médecine Interne et immunologie clinique [CHU Toulouse], Pôle Maladies de l'appareil digestif [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Médecine Interne Onco-hématologie, Centre Hospitalier Général, Service d'Hématologie Clinique [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Department of Haematology, Oncology and Clinical Immunology, Centre for Haematology and Oncology, Heinrich Heine Universität Düsseldorf = Heinrich Heine University [Düsseldorf], Service d'hématologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Hémopathies Myéloïdes : Cellules Souches, Modèles Pré-Cliniques et Recherche Translationnelle (UMR 1131), Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d’Hématologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Université Paris Diderot - Paris 7 (UPD7), Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), CIC - Tours, Centre Hospitalier Régional Universitaire de Tours (CHRU Tours)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d’Investigation Clinique [Tours] CIC 1415 (CIC ), Centre Hospitalier Régional Universitaire de Tours (CHRU Tours)-Hôpital Bretonneau-Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Thrombose : Épidémiologie, Physiopathologie et Thérapeutiques Innovantes (UMR_S 765), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Cochin [AP-HP], Service d'Hématologie clinique et thérapie cellulaire [CHU Limoges], CHU Limoges, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Économie et Statistique (CREST), Ecole Nationale de la Statistique et de l'Analyse de l'Information [Bruz] (ENSAI)-École polytechnique (X)-École Nationale de la Statistique et de l'Administration Économique (ENSAE Paris)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service de Médecine Interne et Immunopathologie, CHU Toulouse [Toulouse], Centre Hospitalier Régional Universitaire de Nancy ( CHRU Nancy ), Heinrich-Heine-Universität Düsseldorf [Düsseldorf], Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Cochin [AP-HP], Hémopathies Myéloïdes : Cellules Souches, Modèles Pré-Cliniques et Recherche Translationnelle, Université Paris Diderot - Paris 7 ( UPD7 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Assistance publique - Hôpitaux de Paris (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], IUH- Institut Universitaire d'hématologie, Université Paris Diderot - Paris 7 ( UPD7 ), CHRU Tours, CHRU Tours-Institut National de la Santé et de la Recherche Médicale ( INSERM ), CIC 1415, Institut National de la Santé et de la Recherche Médicale-Université Francois Rabelais [Tours], Thrombose : Épidémiologie, Physiopathologie et Thérapeutiques Innovantes ( UMR_S 765 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), CHU Cochin [AP-HP], Contrôle de la Réponse Immune B et des Lymphoproliférations ( CRIBL ), Université de Limoges ( UNILIM ) -Génomique, Environnement, Immunité, Santé, Thérapeutique ( GEIST FR CNRS 3503 ) -Centre National de la Recherche Scientifique ( CNRS ), Centre de Recherche en Économie et Statistique ( CREST ), Ecole Nationale de la Statistique et de l'Analyse de l'Information [Bruz] ( ENSAI ) -École polytechnique ( X ) -École Nationale de la Statistique et de l'Administration Économique ( ENSAE ParisTech ), Centre de Recherche en Cancérologie de Marseille ( CRCM ), Aix Marseille Université ( AMU ) -Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Cochin [AP-HP], Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Francois Rabelais [Tours], Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503), Ecole Nationale de la Statistique et de l'Analyse de l'Information [Bruz] (ENSAI)-École polytechnique (X)-École Nationale de la Statistique et de l'Administration Économique (ENSAE ParisTech )-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), and Centre Hospitalier Régional Universitaire de Tours (CHRU Tours)-Hôpital Bretonneau-Université de Tours-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Pediatrics, medicine.medical_specialty, classifications, diagnostic haematology, MDS, neutropenia, thrombocytopenia, Hematology, business.industry, Myelodysplastic syndromes, Neutropenia, medicine.disease, World health, 3. Good health, [ SDV.MHEP.MI ] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, 03 medical and health sciences, 0302 clinical medicine, Refractory, Dysplasia, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, 030220 oncology & carcinogenesis, Immunology, medicine, Young adult, business, ComputingMilieux_MISCELLANEOUS, 030215 immunology
Abstract

International audience; no abstract

Published
2016
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6. Azacitidine for the treatment of lower risk myelodysplastic syndromes : a retrospective study of 74 patients enrolled in an Italian named patient program

Author

Musto, Pellegrino, Maurillo, Luca, Spagnoli, Alessandra, Gozzini, Antonella, Rivellini, Flavia, Lunghi, Monia, Villani, Oreste, Aloe Spiriti, Maria Antonietta, Venditti, Adriano, Santini, Valeria, Leone, Giuseppe, Voso, Maria Teresa, D'Arco, Alfonso Maria, Tatarelli, Caterina, Ferrero, Dario, Gaidano, Gianluca, Palumbo, Giuseppe, Di Raimondo, Francesco, Oliva, Esther, Sanpaolo, Grazia, Tonso, Anna, Santagostino, Alberto, Filardi, Nunzio, Pollio, Berardino, Candoni, Anna, Fili, Carla, Russo, Domenico, Orciuolo, Enrico, Petrini, Mario, Ciuffreda, Lucia, Riezzo, Antonio, Morabito, Fortunato, Mazza, Patrizio, Pastore, Domenico, Specchia, Giorgina, and Ferrara, Felicetto

Subjects
Azacitidine, Hypomethylating agents, International prognostic, Myelodysplastic syndromes, Prognosis, Scoring system, Transfusion, Adult, Aged, Aged, 80 and over, Antimetabolites, Antineoplastic, Drug Evaluation, Female, Humans, Italy, Male, Middle Aged, Myelodysplastic Syndromes, Retrospective Studies, Risk, Treatment Outcome, Cancer Research, Oncology, Antimetabolites, 80 and over, hypomethylating agents, Antineoplastic, myelodysplastic syndromes, International Prognostic Scoring System, medicine.drug, medicine.medical_specialty, azacitidine, medicine.drug_class, Lower risk, Antimetabolite, Internal medicine, azacitidine,hypomethylating agents,myelodysplastic syndromes,prognosis,International Prognostic Scoring System,transfusion, medicine, Risk factor, Adverse effect, transfusion, business.industry, Retrospective cohort study, medicine.disease, Surgery, prognosis, business, Settore MED/15 - Malattie del Sangue
Abstract

BACKGROUND: Azacitidine induces responses and prolongs overall survival compared with conventional care regimens in patients who have high-risk myelodysplastic syndromes (MDS). However, limited data are available concerning the efficacy and safety of azacitidine in patients who have lower risk MDS. METHODS: The authors retrospectively evaluated 74 patients with International Prognostic Scoring System low-risk or intermediate 1-risk MDS, who received azacitidine on a national named patient program. At baseline, 84% of patients were transfusion-dependent, 57% had received erythropoietin, and 51% were aged > 70 years. Azacitidine was administered subcutaneously for 5 days (n ¼ 29 patients), 7 days (n ¼ 43 patients), or 10 days (n ¼ 2 patients) every month at a dose of 75 mg/m2 daily (n ¼ 45 patients) or at a fixed dose of 100 mg daily (n ¼ 29 patients) and for a median of 7 cycles (range, 1-30 cycles). RESULTS: According to the 2006 International Working Group criteria, overall response rate (ORR) was 45.9%, including complete responses (10.8%), partial responses (9.5%), hematologic improvements (20.3%), and bone marrow complete responses (5.4%).The ORR was 51.6% in 64 patients who completed at least 4 cycles of treatment. The median duration of response was 6 months (range, 1-30 months). After a median follow-up of 15 months, 71% of patients remained alive. A survival benefit was observed in responders versus nonresponders (94% vs 54% of patients projected to be alive at 2.5 years, respectively; P < .0014). The most common grade 3 or 4 adverse events were myelosuppression (21.6%) and infection (6.8%). CONCLUSIONS: The current results indicated that azacitidine may be a feasible and effective treatment for patients with lower risk MDS.

Published
2010

7. Hydroxyurea Treatment In 1075 Patients with Essential Thrombocythemia and Occurrence of Extra-Hematological Adverse Events: A Preliminary Report of the Registro Italiano Trombocitemia (RIT)

Author

Luigi Gugliotta, Md1, Papayannidis, Cristina, Piccin, Andrea, Tieghi, Alessia, Vianelli, Nicola, Scalzulli, Potito Rosario, Candoni, Anna, M. D, Md, Dragani, Alfredo, Patriarca, Andrea, Lunghi, Monia, Ciancia, Rosanna, Martinelli, Vincenzo, Liberati, Anna Marina, Specchia, Giorgina, Imovilli, Annalisa, Vannucchi, Alessandro M., Gaetano, Rosa Di, Randi, Maria Luigia, Passamonti, Francesco, Palmieri, Fausto, Mazzucconi, Maria Gabriella, Mastrullo, Lucia, Cimino, Giuseppe, Pierri, Ivana, Cacciola, Emma, Lucchesi, Alessandro, Luraschi, Annalisa, Baccarani, Giovanni Martinelli2, and Michele

Published
2010

8. Aberrant somatic hypermutation in transformation of follicular lymphoma and chronic lymphocytic leukemia to diffuse large B-cell lymphoma

Author

Rossi, Davide, Berra, Eva, Cerri, Michaela, Deambrogi, Clara, Barbieri, Caterina, Franceschetti, Silvia, Lunghi, Monia, Conconi, Annarita, Paulli, Marco, Matolcsy, Andras, Pasqualucci, Laura, Daniela Capello, and Gaidano, Gianluca

Subjects
Gene Rearrangement, Neoplastic, Leukemia, Lymphoma, B-Cell, Lymphoma, B-Lymphocyte, B-Cell, Follicular, Cell Transformation, Somatic Hypermutation, Leukemia, Lymphocytic, Chronic, B-Cell, Lymphocytic, Gene Frequency, Humans, Chronic, Immunoglobulin, Cell Transformation, Neoplastic, Somatic Hypermutation, Immunoglobulin, Gene Rearrangement, B-Lymphocyte, Lymphoma, Follicular
Abstract

The molecular mechanisms involved in histologic transformation of follicular lymphoma (FL) and B-chronic lymphocytic leukemia (B-CLL) to diffuse large B-cell lymphoma (DLBCL) are heterogeneous and largely unknown. Here we explored whether aberrant somatic hypermutation, leading to the acquisition of new mutations in PIM-1, PAX-5, RhoH/TTF and c-MYC genes, is involved in transformation from FL or B-CLL to DLBCL. Eighteen sequential pairs of FL/DLBCL (n=9) and B-CLL/DLBCL (n=9) were investigated. Our findings demonstrate that acquisition of novel mutations due to aberrant somatic hypermutation was associated with DLBCL transformation in 5/9 (55.5%) cases of FL and 2/9 (22.2%) cases of B-CLL.

Published
2006

9. A Preliminary Analysis of FLAM (Italian Non-Interventional Multi-Center Study of FLT3-Mutated AML Patients): FLT3 Receptor Gene Mutational Analysis and FLT3 Inhibitor Administration in Real-Life Clinical Practice

Author

Nanni, Jacopo, Audisio, Ernesta, Giannini, Maria Benedetta, Scappini, Barbara, Cambo, Benedetta, Albano, Francesco, Martelli, Maria Paola, Cignetti, Alessandro, Rigolin, Gian Matteo, Fracchiolla, Nicola, Bocchia, Monica, Romani, Claudio, Todisco, Elisabetta, Lunghi, Monia, Mianulli, Annamaria, Cilloni, Daniela, Petracci, Elisabetta, Valli, Irene, Zingaretti, Chiara, Cerchione, Claudio, Cangini, Delia, CRISTINA PAPAYANNIDIS, and Martinelli, Giovanni

10. INCB84344-201: Ponatinib and steroids in frontline therapy for unfit patients with Ph+ acute lymphoblastic leukemia

Author

Carolina Terragna, Maria Paola Martelli, Paolo de Fabritiis, Anna Candoni, Alessandra Tedeschi, Giovanni Martinelli, Monia Lunghi, Stefania Paolini, Michele Baccarani, Alfonso Piciocchi, Francesco Fabbiano, Luca Frison, Monica Bocchia, Antonella Vitale, Antonella Fornaro, Cristina Papayannidis, Antonio Cuneo, Piero Galieni, Muriel Granier, Mingyue Wang, Michele Cavo, Robin Foà, Paola Fazi, Marco Vignetti, Chiara Sartor, Roberto M. Lemoli, Fabio Guolo, Simona Soverini, Carmine Selleri, Mariachiara Abbenante, Valentina Robustelli, Giovanni Marconi, Federico Simonetti, Silvia Trappolini, Massimiliano Bonifacio, Patrizia Tosi, Stefano D'Ardia, Zhaoyin Zhu, Martinelli, Giovanni, Papayannidis, Cristina, Piciocchi, Alfonso, Robustelli, Valentina, Soverini, Simona, Terragna, Carolina, Marconi, Giovanni, Lemoli, Roberto Massimo, Guolo, Fabio, Fornaro, Antonella, Lunghi, Monia, de Fabritiis, Paolo, Candoni, Anna, Selleri, Carmine, Simonetti, Federico, Bocchia, Monica, Vitale, Antonella, Frison, Luca, Tedeschi, Alessandra, Cuneo, Antonio, Bonifacio, Massimiliano, Martelli, Maria Paola, D'Ardia, Stefano, Trappolini, Silvia, Tosi, Patrizia, Galieni, Piero, Fabbiano, Francesco, Abbenante, Maria Chiara, Granier, Muriel, Zhu, Zhaoyin, Wang, Mingyue, Sartor, Chiara, Paolini, Stefania, Cavo, Michele, Foà, Robin, Fazi, Paola, Vignetti, Marco, and Baccarani, Michele

Subjects
medicine.medical_specialty, Population, Gastroenterology, Disease-Free Survival, chemistry.chemical_compound, Prednisone, Internal medicine, Antineoplastic Combined Chemotherapy Protocols, Tyrosine kinase inhibitors, Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL), GIMEMA LAL 1811, medicine, Clinical endpoint, Humans, Philadelphia Chromosome, Prospective Studies, education, Adverse effect, Aged, education.field_of_study, biology, business.industry, Ponatinib, Imidazoles, Hematology, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Settore MED/15, Rash, Pyridazines, Transplantation, chemistry, Alanine transaminase, biology.protein, medicine.symptom, business, medicine.drug
Abstract

Tyrosine kinase inhibitors have improved survival for patients with Philadelphia chromosome–positive (Ph+) acute lymphoblastic leukemia (ALL). However, prognosis for old or unfit patients remains poor. In the INCB84344-201 (formerly GIMEMA LAL 1811) prospective, multicenter, phase 2 trial, we tested the efficacy and safety of ponatinib plus prednisone in newly diagnosed patients with Ph+ ALL ≥60 years, or unfit for intensive chemotherapy and stem cell transplantation. Forty-four patients received oral ponatinib 45 mg/d for 48 weeks (core phase), with prednisone tapered to 60 mg/m2/d from days-14-29. Prophylactic intrathecal chemotherapy was administered monthly. Median age was 66.5 years (range, 26-85). The primary endpoint (complete hematologic response [CHR] at 24 weeks) was reached in 38/44 patients (86.4%); complete molecular response (CMR) in 18/44 patients (40.9%) at 24 weeks. 61.4% of patients completed the core phase. As of 24 April 2020, median event-free survival was 14.31 months (95% CI 9.30-22.31). Median overall survival and duration of CHR were not reached; median duration of CMR was 11.6 months. Most common treatment-emergent adverse events (TEAEs) were rash (36.4%), asthenia (22.7%), alanine transaminase increase (15.9%), erythema (15.9%), and γ-glutamyltransferase increase (15.9%). Cardiac and vascular TEAEs occurred in 29.5% (grade ≥3, 18.2%) and 27.3% (grade ≥3, 15.9%), respectively. Dose reductions, interruptions, and discontinuations due to TEAEs occurred in 43.2%, 43.2%, and 27.3% of patients, respectively; 5 patients had fatal TEAEs. Ponatinib and prednisone showed efficacy in unfit patients with Ph+ ALL; however, a lower ponatinib dose may be more appropriate in this population. This trial was registered at www.clinicaltrials.gov as #NCT01641107.

Published
2022

11. Decreased function of Fas and variations of the perforin gene in adult patients with primary immune thrombocytopenia

Author

Nausicaa Clemente, Renato Fanin, Monia Lunghi, Simona Puglisi, Davide Rossi, Gianluca Gaidano, Nicola Vianelli, Giuseppe Cappellano, Michaela Cerri, Elena Boggio, Annalisa Chiocchetti, Eleonora Toffoletti, Cristoforo Comi, Eloise Beggiato, Umberto Dianzani, Casimiro Luca Gigliotti, Francesco Zaja, Silvia Cantoni, Alessia Tieghi, Boggio, Elena, Gigliotti, Casimiro L., Rossi, Davide, Toffoletti, Eleonora, Cappellano, Giuseppe, Clemente, Nausicaa, Puglisi, Simona, Lunghi, Monia, Cerri, Michaela, Vianelli, Nicola, Cantoni, Silvia, Tieghi, Alessia, Beggiato, Eloise, Gaidano, Gianluca, Comi, Cristoforo, Chiocchetti, Annalisa, Fanin, Renato, Dianzani, Umberto, and Zaja, Francesco

Subjects
0301 basic medicine, Adult, Male, Myeloid, cytokine secretion, Adolescent, Mutation, Missense, T-Lymphocytes, Regulatory, Autoimmune thrombocytopenia, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Immune system, hemic and lymphatic diseases, PRF1 variation, Medicine, Humans, Myeloid Cells, fas Receptor, Aged, Aged, 80 and over, Fas function, B-Lymphocytes, Purpura, Thrombocytopenic, Idiopathic, business.industry, Perforin, Interleukin-17, PRF1 variations, Interleukin, Hematology, Dendritic Cells, Middle Aged, Fas receptor, medicine.disease, Interleukin-10, Treg, Interleukin 10, 030104 developmental biology, medicine.anatomical_structure, immune thrombocytopenia, ITP, Autoimmune lymphoproliferative syndrome, Immunology, Female, Interleukin 17, business, 030215 immunology
Abstract

A defective switching off of the immune response is involved in several autoimmune diseases. This switching off involves Fas-mediated apoptosis, perforin-mediated fratricide of activated lymphocytes, and the suppressive activity of regulatory T (Treg) cells. These mechanisms are altered in autoimmune lymphoproliferative syndrome that often displays autoimmune thrombocytopenia. The aim of this research was to evaluate these mechanisms in adult patients with primary immune thrombocytopenia (ITP), compared with healthy controls. The results show that a substantial subgroup of the ITP patients displayed a defective Fas function; most of them displayed decreased Fas expression in T cells activated in vitro. Moreover, ITP patients displayed an increased frequency of rare missense variations of the PRF1 gene and decreased levels of Treg. Immunological analysis showed that levels of Interleukin (IL)10 and IL17 were decreased and marginal zone B cells were increased. Moreover, myeloid and plasmacytoid dendritic cells were decreased in ITP patients. In conclusion, in adult ITP patients, several mechanisms involved in shutting off the immune response are defective and several immunological parameters are dysregulated; these alterations may play a role in the clinical heterogeneity of the disease.

Published
2016

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