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26 results on '"Bonifacio, Elisabetta"'

1. Tregs prevent GVHD and promote immune reconstitution in HLA-haploidentical transplantation

Author

Di Ianni, Mauro, Falzetti, Franca, Carotti, Alessandra, Terenzi, Adelmo, Castellino, Flora, Bonifacio, Elisabetta, Del Papa, Beatrice, Zei, Tiziana, Ostini, Roberta Iacucci, Cecchini, Debora, Aloisi, Teresa, Perruccio, Katia, Ruggeri, Loredana, Balucani, Chiara, Pierini, Antonio, Sportoletti, Paolo, Aristei, Cynthia, Falini, Brunangelo, Reisner, Yair, Velardi, Andrea, Aversa, Franco, and Martelli, Massimo F.

Published
2011
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2. CD34+ cells from AML with mutated NPM1 harbor cytoplasmic mutated nucleophosmin and generate leukemia in immunocompromised mice

Author

Martelli, Maria Paola, Pettirossi, Valentina, Thiede, Christian, Bonifacio, Elisabetta, Mezzasoma, Federica, Cecchini, Debora, Pacini, Roberta, Tabarrini, Alessia, Ciurnelli, Raffaella, Gionfriddo, Ilaria, Manes, Nicla, Rossi, Roberta, Giunchi, Linda, Oelschlägel, Uta, Brunetti, Lorenzo, Gemei, Marica, Delia, Mario, Specchia, Giorgina, Liso, Arcangelo, Di Ianni, Mauro, Di Raimondo, Francesco, Falzetti, Franca, Del Vecchio, Luigi, Martelli, Massimo F., and Falini, Brunangelo

Published
2010
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6. NOTCH1 PEST domain mutation is an adverse prognostic factor in B-CLL

Author

Sportoletti, Paolo, Baldoni, Stefano, Cavalli, Laura, Del Papa, Beatrice, Bonifacio, Elisabetta, Ciurnelli, Raffaella, Bell, Alain Sylvin, Di Tommaso, Ambra, Rosati, Emanuela, Crescenzi, Barbara, Mecucci, Cristina, Screpanti, Isabella, Marconi, Pierfrancesco, Martelli, Massimo F., Di Ianni, Mauro, and Falzetti, Franca

Published
2010
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7. Graft engineering for allogeneic haploidentical stem cell transplantation

Author

Tabilio, Antonio, Falzetti, Franca, Zei, Tiziana, De Ioanni, Maria, Bonifacio, Elisabetta, Battelli, Feliciana, Iacucci Ostini, Roberta, Ballanti, Stelvio, Cimminiello, Michele, Capponi, Monia, Silvani, Carla, Minelli, Olivia, Fettucciari, Katia, Marconi, Pierfrancesco, Rosati, Emanuela, Santucci, Antonella, Di Ianni, Mauro, Aversa, Franco, and Martelli, Massimo F.

Published
2004
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8. Nonpeghylated liposomal doxorubicin combination regimen (R‐COMP) for the treatment of lymphoma patients with advanced age or cardiac comorbidity.

Author

Rigacci, Luigi, Annibali, Ombretta, Kovalchuk, Sofya, Bonifacio, Elisabetta, Pregnolato, Francesca, Angrilli, Francesco, Vitolo, Umberto, Pozzi, Samantha, Broggi, Serena, Luminari, Stefano, Merli, Francesco, Spina, Michele, Bolis, Silvia, Margiotta‐Casaluci, Gloria, Scalzulli, Rosario, Cox, Christina, Mamusa, Angela Maria, Santoro, Armando, Zinzani, Pier Luigi, and Ferrari, Samantha

Subjects
CORONARY disease, PROGRESSION-free survival, LYMPHOMAS, PULMONARY edema, HEART diseases
Abstract

Doxorubicin is the most effective single agent in the treatment of non‐Hodgkin's lymphoma (NHL). Its use is limited because of the cardiac toxicity primarily in elderly patients (pts) and in pts with history of cardiac disease. Liposomal doxorubicin has been proven to reduce cardiotoxicity. The aim of this retrospective study was the use of nonpeghylated liposomal doxorubicin (NPLD) in term of efficacy, response rate and incidence of cardiac events. We retrospectively collected the experience of 33 Hematological Italian Centers in using NPLD. Nine hundred and forty‐six consecutive pts treated with R‐COMP (doxorubicin was substituted with NPLD, Myocet) were collected. Median age was 74 years, the reasons for use of NPLD were: age (466 pts), cardiac disease (298 pts), uncontrolled hypertension (126 pts), other reasons (56 pts). According to clinicians' evaluation, 49.9% of pts would not have used standard doxorubicin for different situations (age, cardiomyopathy, previous use of doxorubicin, and uncontrolled hypertension). Overall 687 pts (72.6%) obtained a complete remission (CR). About 5% (n = 51) of subjects developed major cardiotoxic events including heart failure (N = 31), ischemic heart disease (N = 16), acute heart attack (N = 3), and acute pulmonary oedema (N = 1). After a median follow‐up of 32 months, 651 pts were alive and the overall survival (OS) was 72%. After a median observation period of 23 months disease free survival (DFS) was 58%. Either in univariate or in multivariate analysis OS and DFS were not significantly affected by age or cardiac disease. Our findings strongly support that including R‐COMP is effective and safe when the population is at high risk of cardiac events and negatively selected. Moreover, the use of this NPLD permitted that about half of our population had the opportunity to receive the best available treatment. [ABSTRACT FROM AUTHOR]

Published
2020
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9. Dissecting the Hierarchical Level of Hematopoietic Progenitors' Involvement in AML with NPM1 Gene Mutation and Their Engraftment Potential in Immunocompromised Mice.

Author

Martelli, Maria Paola, primary, Pettirossi, Valentina, additional, Thiede, Christian, additional, Bonifacio, Elisabetta, additional, Ianni, Mauro Di, additional, Gionfriddo, Ilaria, additional, Cecchini, Debora, additional, Pacini, Roberta, additional, Tabarrini, Alessia, additional, Mezzasoma, Federica, additional, Rossi, Roberta, additional, Giunchi, Linda, additional, Oelschlägel, Uta, additional, Brunetti, Lorenzo, additional, Gemei, Marica, additional, Ciurnelli, Raffaella, additional, Cecchetti, Federica, additional, Carolis, Luca De, additional, Liso, Arcangelo, additional, Raimondo, Francesco Di, additional, Martelli, Massimo F, additional, and Falini, Brunangelo, additional

Published
2009
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10. Acute Myeloid Leukemia with Mutated NPM1 Presenting with Life-Threatening, Either Arterial or Venous, Thromboembolism: a Report of 4 Cases.

Author

Martelli, Maria Paola, primary, Brunetti, Lorenzo, additional, De Carolis, Luca, additional, Agliani, Elisabetta, additional, Berchicci, Laura, additional, Bonifacio, Elisabetta, additional, Pettirossi, Valentina, additional, Gionfriddo, Ilaria, additional, Cecchini, Debora, additional, Tabarrini, Alessia, additional, Rossi, Roberta, additional, Ballanti, Stelvio, additional, Martelli, Massimo F, additional, and Falini, Brunangelo, additional

Published
2009
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12. Evidence for CD34+ Hematopoietic Progenitor Cell Involvement in Acute Myeloid Leukemia with NPM1 Gene Mutation: Implications for the Cell of Origin

Author

Martelli, Maria Paola, primary, Pettirossi, Valentina, primary, Bonifacio, Elisabetta, primary, Mezzasoma, Federica, primary, Manes, Nicla, primary, Cecchini, Debora, primary, Capanni, Maruska, primary, Gionfriddo, Ilaria, primary, Liso, Arcangelo, primary, Pacini, Roberta, primary, Carini, Manola, primary, Specchia, Giorgina, primary, Martelli, Massimo F, primary, and Falini, Brunangelo, primary

Published
2008
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17. Reciprocal Interaction between NPM Leukemic Mutants and Arf: Structural Basis and Functional Consequences.

Author

Bolli, Niccolo’, primary, Paola Martelli, Maria, additional, Bigerna, Barbara, additional, Pucciarini, Alessandra, additional, Verducci, Barbara, additional, Pallotta, Teresa, additional, de Marco, Felicetta, additional, Pettirossi, Valentina, additional, Mannucci, Roberta, additional, Bonifacio, Elisabetta, additional, Tabilio, Antonio, additional, Nicoletti, Ildo, additional, and Falini, Brunangelo, additional

Published
2006
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18. Unique human CD133+ leukemia cell line and its modulation towards a mesenchymal phenotype by FGF2 and TGFβ1

Author

Bodo, Maria, primary, Baroni, Tiziano, additional, Bellucci, Catia, additional, Lilli, Cinzia, additional, De Ioanni, Maria, additional, Bonifacio, Elisabetta, additional, Moretti, Lorenzo, additional, Becchetti, Ennio, additional, Bellocchio, Silvia, additional, Delfini, Costante, additional, Lumare, Eleonora, additional, and Tabilio, Antonio, additional

Published
2005
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19. Interleukin 7-Engineered Stromal Cells: A New Approach for Hastening Naive T Cell Recruitment

Author

Di Ianni, Mauro, primary, Papa, Beatrice Del, additional, De Ioanni, Maria, additional, Terenzi, Adelmo, additional, Sportoletti, Paolo, additional, Moretti, Lorenzo, additional, Falzetti, Franca, additional, Gaozza, Eugenia, additional, Zei, Tiziana, additional, Spinozzi, Fabrizio, additional, Bagnis, Claude, additional, Mannoni, Patrice, additional, Bonifacio, Elisabetta, additional, Falini, Brunangelo, additional, Martelli, Massimo F., additional, and Tabilio, Antonio, additional

Published
2005
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20. Unique human CD133+ leukemia cell line and its modulation towards a mesenchymal phenotype by FGF2 and TGFβ1<FNR></FNR><FN>Maria Bodo and Tiziano Baroni have contributed equally to this study. </FN>.

Author

Bodo, Maria, Baroni, Tiziano, Bellucci, Catia, Lilli, Cinzia, De Ioanni, Maria, Bonifacio, Elisabetta, Moretti, Lorenzo, Becchetti, Ennio, Bellocchio, Silvia, Delfini, Costante, Lumare, Eleonora, and Tabilio, Antonio

Subjects
LYMPHOBLASTIC leukemia, CELL lines, MESSENGER RNA, FIBRONECTINS, GLYCOSAMINOGLYCANS, PROTEOGLYCANS, POLYMERASE chain reaction, NERVE growth factor
Abstract

Immunological features of GM-490 cells, a new blood cell line from a patient with acute lymphoblastic leukemia, included lack of CD34, CD38, CD45, CD14, HLA-DR, and lymphoid and myeloid markers and expression of CD29, CD36, CD44, CD54, CD71, CD105, and CD133. Molecular analysis indicated CD45 gene expression was absent but CD34 mRNA was present. GM-490 cells constitutively produced fibronectin (FN), type III and traces of type I collagen, collagenases, glycosaminoglycans (GAG) and biglycan and betaglycan proteoglycans (PG) as well as FGF2 and TGFβ1. When FGF2 and/or TGFβ1 were added to cells in vitro, they stimulated cell proliferation and differently modulated matrix production and growth factor receptor expression. Reverse transcription-polymerase chain reaction (RT-PCR) detection of transcripts encoding for osteocalcin and RUNX2 suggests GM-490 cells differentiate towards the osteoblast pathway. GM-490 cells expressed the low affinity nerve growth factor receptor (p75LNGFR), a somatic stem cell marker that is not detected in hematopoietic cells, leading to the hypothesis that GM-490 has mesenchymal stem cell properties. The reciprocal modulating effects of FGF2 and TGFβ1 on each other's receptors make the GM-490 cell line a new model for investigating the relationship between these growth factors and their receptors in autocrine loops which are believed to sustain the malignant clone in hematological diseases. © 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Published
2006
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21. CD34+cells from AML with mutated NPM1harbor cytoplasmic mutated nucleophosmin and generate leukemia in immunocompromised mice

Author

Martelli, Maria Paola, Pettirossi, Valentina, Thiede, Christian, Bonifacio, Elisabetta, Mezzasoma, Federica, Cecchini, Debora, Pacini, Roberta, Tabarrini, Alessia, Ciurnelli, Raffaella, Gionfriddo, Ilaria, Manes, Nicla, Rossi, Roberta, Giunchi, Linda, Oelschlägel, Uta, Brunetti, Lorenzo, Gemei, Marica, Delia, Mario, Specchia, Giorgina, Liso, Arcangelo, Di Ianni, Mauro, Di Raimondo, Francesco, Falzetti, Franca, Del Vecchio, Luigi, Martelli, Massimo F., and Falini, Brunangelo

Abstract

Acute myeloid leukemia (AML) with mutated NPM1shows distinctive biologic and clinical features, including absent/low CD34 expression, the significance of which remains unclear. Therefore, we analyzed CD34+cells from 41 NPM1-mutated AML. At flow cytometry, 31 of 41 samples contained less than 10% cells showing low intensity CD34 positivity and variable expression of CD38. Mutational analysis and/or Western blotting of purified CD34+cells from 17 patients revealed NPM1-mutated gene and/or protein in all. Immunohistochemistry of trephine bone marrow biopsies and/or flow cytometry proved CD34+leukemia cells from NPM1-mutated AML had aberrant nucleophosmin expression in cytoplasm. NPM1-mutated gene and/or protein was also confirmed in a CD34+subfraction exhibiting the phenotype (CD34+/CD38−/CD123+/CD33+/CD90−) of leukemic stem cells. When transplanted into immunocompromised mice, CD34+cells generated a leukemia recapitulating, both morphologically and immunohistochemically (aberrant cytoplasmic nucleophosmin, CD34 negativity), the original patient's disease. These results indicate that the CD34+fraction in NPM1-mutated AML belongs to the leukemic clone and contains NPM1-mutated cells exhibiting properties typical of leukemia-initiating cells. CD34−cells from few cases (2/15) also showed significant leukemia-initiating cell potential in immunocompromised mice. This study provides further evidence that NPM1mutation is a founder genetic lesion and has potential implications for the cell-of-origin and targeted therapy of NPM1-mutated AML.

Published
2010
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22. Dissecting the Hierarchical Level of Hematopoietic Progenitors' Involvement in AML with NPM1Gene Mutation and Their Engraftment Potential in Immunocompromised Mice.

Author

Martelli, Maria Paola, Pettirossi, Valentina, Thiede, Christian, Bonifacio, Elisabetta, Ianni, Mauro Di, Gionfriddo, Ilaria, Cecchini, Debora, Pacini, Roberta, Tabarrini, Alessia, Mezzasoma, Federica, Rossi, Roberta, Giunchi, Linda, Oelschlägel, Uta, Brunetti, Lorenzo, Gemei, Marica, Ciurnelli, Raffaella, Cecchetti, Federica, Carolis, Luca De, Liso, Arcangelo, Raimondo, Francesco Di, Martelli, Massimo F, and Falini, Brunangelo

Abstract

Abstract 480

Published
2009
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24. Evidence for CD34+ Hematopoietic Progenitor Cell Involvement in Acute Myeloid Leukemia with NPM1Gene Mutation: Implications for the Cell of Origin

Author

Martelli, Maria Paola, Pettirossi, Valentina, Bonifacio, Elisabetta, Mezzasoma, Federica, Manes, Nicla, Cecchini, Debora, Capanni, Maruska, Gionfriddo, Ilaria, Liso, Arcangelo, Pacini, Roberta, Carini, Manola, Specchia, Giorgina, Martelli, Massimo F, and Falini, Brunangelo

Abstract

Acute myeloid leukemia expressing mutated NPM1gene and cytoplasmic nucleophosmin (NPMc+ AML) [Falini B et al, NEJM 2005; 352:254–266] is a new entity of WHO classification that shows distinctive biological and clinical features, including a unique molecular signature characterized by downregulation of CD34 and upregulation of most HOXgenes [Falini B et al, Blood 2007; 109:874–885]. Involvement of HOXgenes in the maintenance of the stem-cell phenotype strongly suggest that AML with mutated NPM1originates from a multipotent hematopoietic progenitor (HSC). This view is also supported by immunohistological findings showing that AML with mutated NPM1frequently displays multilineage involvement [Pasqualucci L et al, Blood 2006; 108:4146–4155]. On the other hand, the frequent negativity of NPMc+ AML for the HSC-associated antigen CD34 raises the question of whether the mutation event occurs in a CD34-negative HSC (these cells have been identified in mice) or whether a minimal pool of CD34-positive NPM1-mutated leukemic cells does exist. Currently, the hierarchical level of stem cell involvement in NPMc+ AML is unknown. To address this issue, we purified CD34+ cells from NPMc+ AML patients and detected NPM1 mutant protein in the sorted population by Western blot with anti-NPM mutant specific antibodies [Martelli MP et al, Leukemia2008] (Figure 1A). We investigated 6 NPMc+ AML patients presenting at diagnosis with 0.12%, 0.14%, 0.38%, 5%, 22%, and 28% of CD34+ cells in the peripheral blood. In all cases, CD34+ fractions (purity >90%) harboured NPM1 mutant protein, indicating they belong to the leukemic clone (Figure 1B). The percentage of most undifferentiated CD34+/CD38− cells in the CD34+ fractions ranged from 5 to 97%. Notably, in at least one case, all CD34+ NPM1-mutated leukemic cells were CD38−negative. Moreover in all cases, CD34+ NPM1-mutated leukemic cells appeared to express CD123 (IL-3 receptor), considered a marker of the leukemic stem cell and target of potential therapy. Double staining of bone marrow biopsies with anti-CD34 and anti-NPM antibodies revealed that the rare CD34+ cells expressed NPM1 aberrantly in the cytoplasm. Inoculation of CD34+ NPM1-mutated AML cells into sublethally irradiated NOD/SCID mice resulted into leukemia engrafment in various body sites, especially bone marrow, spleen, lung and liver. Preliminary results showed that CD34+ leukemic cells reacquired the same leukemic phenotype as the original patient's, including CD34-negativity of the leukemic bulk in spite of any lack of differentiation. This finding suggests that NPM1 mutant protein may be involved in downregulation of CD34 antigen, while keeping a gene expression profile typical of the hematopoietic stem cell. These findings suggest the CD34+ fraction contains the SCID-leukemia initiating cells (SL-IC) and point to CD34+/CD38− HSC as the cell of origin of AML with mutated NPM1.

Published
2008
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25. Are ongoing trials on hematologic malignancies still excluding older subjects?

Author

Cherubini A, Pierri F, Gasperini B, Zengarini E, Cerenzia A, Bonifacio E, Falcinelli F, and Lattanzio F

Subjects
Age Factors, Aged, Hematologic Neoplasms diagnosis, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive diagnosis, Leukemia, Myelogenous, Chronic, BCR-ABL Positive therapy, Myelodysplastic Syndromes diagnosis, Myelodysplastic Syndromes therapy, Myelodysplastic-Myeloproliferative Diseases diagnosis, Myelodysplastic-Myeloproliferative Diseases therapy, Registries, World Health Organization, Hematologic Neoplasms blood, Hematologic Neoplasms therapy, Patient Selection, Randomized Controlled Trials as Topic methods, Randomized Controlled Trials as Topic trends
Published
2013
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26. Unique human CD133+ leukemia cell line and its modulation towards a mesenchymal phenotype by FGF2 and TGFbeta1.

Author

Bodo M, Baroni T, Bellucci C, Lilli C, De Ioanni M, Bonifacio E, Moretti L, Becchetti E, Bellocchio S, Delfini C, Lumare E, and Tabilio A

Subjects
AC133 Antigen, Animals, Bone Marrow Cells drug effects, Cell Differentiation, Cell Proliferation drug effects, Collagen biosynthesis, Collagenases metabolism, Colony-Forming Units Assay, Core Binding Factor Alpha 1 Subunit metabolism, Fibroblast Growth Factor 2 metabolism, Fibronectins biosynthesis, Glycosaminoglycans biosynthesis, Humans, Osteocalcin metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma, RNA, Messenger metabolism, Receptor, Fibroblast Growth Factor, Type 2 metabolism, Receptor, Nerve Growth Factor metabolism, Transforming Growth Factor beta metabolism, Antigens, CD metabolism, Bone Marrow Cells physiology, Cell Line, Tumor, Fibroblast Growth Factor 2 pharmacology, Glycoproteins metabolism, Mesenchymal Stem Cells physiology, Peptides metabolism, Transforming Growth Factor beta pharmacology
Abstract

Immunological features of GM-490 cells, a new blood cell line from a patient with acute lymphoblastic leukemia, included lack of CD34, CD38, CD45, CD14, HLA-DR, and lymphoid and myeloid markers and expression of CD29, CD36, CD44, CD54, CD71, CD105, and CD133. Molecular analysis indicated CD45 gene expression was absent but CD34 mRNA was present. GM-490 cells constitutively produced fibronectin (FN), type III and traces of type I collagen, collagenases, glycosaminoglycans (GAG) and biglycan and betaglycan proteoglycans (PG) as well as FGF2 and TGFbeta1. When FGF2 and/or TGFbeta1 were added to cells in vitro, they stimulated cell proliferation and differently modulated matrix production and growth factor receptor expression. Reverse transcription-polymerase chain reaction (RT-PCR) detection of transcripts encoding for osteocalcin and RUNX2 suggests GM-490 cells differentiate towards the osteoblast pathway. GM-490 cells expressed the low affinity nerve growth factor receptor (p75LNGFR), a somatic stem cell marker that is not detected in hematopoietic cells, leading to the hypothesis that GM-490 has mesenchymal stem cell properties. The reciprocal modulating effects of FGF2 and TGFbeta1 on each other's receptors make the GM-490 cell line a new model for investigating the relationship between these growth factors and their receptors in autocrine loops which are believed to sustain the malignant clone in hematological diseases., (Copyright 2005 Wiley-Liss, Inc.)

Published
2006
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