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10 results on '"Bartalucci A"'

1. Chromosome 9p trisomy increases stem cells clonogenic potential and fosters T-cell exhaustion in JAK2-mutant myeloproliferative neoplasms

Author

Carretta, Chiara, Parenti, Sandra, Bertesi, Matteo, Rontauroli, Sebastiano, Badii, Filippo, Tavernari, Lara, Genovese, Elena, Malerba, Marica, Papa, Elisa, Sperduti, Samantha, Enzo, Elena, Mirabile, Margherita, Pedrazzi, Francesca, Neroni, Anita, Tombari, Camilla, Mora, Barbara, Maffioli, Margherita, Mondini, Marco, Brociner, Marco, Maccaferri, Monica, Tenedini, Elena, Martinelli, Silvia, Bartalucci, Niccolò, Bianchi, Elisa, Casarini, Livio, Potenza, Leonardo, Luppi, Mario, Tagliafico, Enrico, Guglielmelli, Paola, Simoni, Manuela, Passamonti, Francesco, Norfo, Ruggiero, Vannucchi, Alessandro Maria, and Manfredini, Rossella

Published
2024
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3. Inhibition of ERK1/2 signaling prevents bone marrow fibrosis by reducing osteopontin plasma levels in a myelofibrosis mouse model

Author

Bianchi, Elisa, Rontauroli, Sebastiano, Tavernari, Lara, Mirabile, Margherita, Pedrazzi, Francesca, Genovese, Elena, Sartini, Stefano, Dall’Ora, Massimiliano, Grisendi, Giulia, Fabbiani, Luca, Maccaferri, Monica, Carretta, Chiara, Parenti, Sandra, Fantini, Sebastian, Bartalucci, Niccolò, Calabresi, Laura, Balliu, Manjola, Guglielmelli, Paola, Potenza, Leonardo, Tagliafico, Enrico, Losi, Lorena, Dominici, Massimo, Luppi, Mario, Vannucchi, Alessandro Maria, and Manfredini, Rossella

Published
2023
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7. GIPSS: genetically inspired prognostic scoring system for primary myelofibrosis

Author

Kebede H. Begna, Christy Finke, Curtis A. Hanson, Mythri Mudireddy, Ayalew Tefferi, Francesco Mannelli, Terra L. Lasho, Alessandro M. Vannucchi, Rhett P. Ketterling, Null Naseema Gangat, Animesh Pardanani, Niccolò Bartalucci, Paola Guglielmelli, and Maura Nicolosi

Subjects
Oncology, Adult, Male, Cancer Research, medicine.medical_specialty, Scoring system, Risk Assessment, Article, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Internal medicine, Medicine, Humans, Genetic Predisposition to Disease, Genetic risk, Myelofibrosis, Survival analysis, Prognostic models, Genetic Association Studies, Aged, business.industry, Epistasis, Genetic, Hematology, Middle Aged, medicine.disease, Prognosis, Survival Analysis, Cell Transformation, Neoplastic, Genetic marker, Primary Myelofibrosis, 030220 oncology & carcinogenesis, Mutation (genetic algorithm), Female, business, Risk assessment, Biomarkers, 030215 immunology
Abstract

International collaborations over the years have produced a series of prognostic models for primary myelofibrosis (PMF), including the recently unveiled mutation-enhanced international prognostic scoring systems for transplant-age patients (MIPSS70 and MIPSS70-plus). In the current study, we considered the feasibility of a genetically inspired prognostic scoring system (GIPSS) that is exclusively based on genetic markers. Among 641 cytogenetically annotated patients with PMF and informative for previously recognized adverse mutations, multivariable analysis identified “VHR” karyotype, “unfavorable” karyotype, absence of type 1/like CALR mutation and presence of ASXL1, SRSF2, or U2AF1Q157 mutation, as inter-independent predictors of inferior survival; the respective HRs (95% CI) were 3.1 (2.1–4.3), 2.1 (1.6–2.7), 2.1 (1.6–2.9), 1.8 (1.5–2.3), 2.4 (1.9–3.2), and 2.4 (1.7–3.3). Based on HR-weighted risk points, a four-tiered GIPSS model was devised: low (zero points; n = 58), intermediate-1 (1 point; n = 260), intermediate-2 (2 points; n = 192), and high (≥3 points; n = 131); the respective median (5-year) survivals were 26.4 (94%), 8.0 (73%), 4.2 (40%), and 2 (14%) years; the model was internally validated by bootstrapping and its predictive accuracy was shown to be comparable to that of MIPSS70-plus. GIPPS offers a low-complexity prognostic tool for PMF that is solely dependent on genetic risk factors and, thus, forward-looking in its essence.

Published
2018

8. No role for CXCL12–G801A polymorphism in the development of extramedullary disease in acute myeloid leukemia

Author

Elisabetta Antonioli, Francesco Mannelli, Niccolò Bartalucci, Alberto Bosi, Stefania Ciolli, Giacomo Gianfaldoni, Vanessa Ponziani, Paola Guglielmelli, Franco Leoni, and Alessandro M. Vannucchi

Subjects
Adult, Male, Receptors, CXCR4, Cancer Research, Disease free survival, Adolescent, Genotype, CD34, Biology, Polymorphism, Single Nucleotide, Disease-Free Survival, Remission induction, hemic and lymphatic diseases, Antineoplastic Combined Chemotherapy Protocols, Humans, Sarcoma, Myeloid, Alleles, Survival analysis, Aged, Proportional Hazards Models, Aged, 80 and over, Remission Induction, Myeloid leukemia, Hematology, Middle Aged, Survival Analysis, Chemokine CXCL12, biological factors, Neoplasm Proteins, Oncology, Extramedullary disease, Leukemia, Myeloid, Acute Disease, embryonic structures, Immunology, Female, biological phenomena, cell phenomena, and immunity
Abstract

No role for CXCL12–G801A polymorphism in the development of extramedullary disease in acute myeloid leukemia

Published
2007

9. Involvement of MAF/SPP1 axis in the development of bone marrow fibrosis in PMF patients

Author

Ruberti, S, Bianchi, E, Guglielmelli, P, Rontauroli, S, Barbieri, G, Tavernari, L, Fanelli, T, Norfo, R, Pennucci, V, Fattori, G Corbizi, Mannarelli, C, Bartalucci, N, Mora, B, Elli, L, Avanzini, M A, Rossi, C, Salmoiraghi, S, Zini, R, Salati, S, Prudente, Z, Rosti, V, Passamonti, F, Rambaldi, A, Ferrari, S, Tagliafico, E, Vannucchi, A M, and Manfredini, R

Abstract

Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hyperplastic megakaryopoiesis and myelofibrosis. We recently described the upregulation of MAF (v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog) in PMF CD34+ hematopoietic progenitor cells (HPCs) compared to healthy donor. Here we demonstrated that MAF is also upregulated in PMF compared with the essential thrombocytemia (ET) and polycytemia vera (PV) HPCs. MAF overexpression and knockdown experiments shed some light into the role of MAF in PMF pathogenesis, by demonstrating that MAF favors the megakaryocyte and monocyte/macrophage commitment of HPCs and leads to the increased expression of proinflammatory and profibrotic mediators. Among them, we focused our further studies on SPP1 and LGALS3. We assessed SPP1 and LGALS3 protein levels in 115 PMF, 47 ET and 24 PV patients plasma samples and we found that SPP1 plasma levels are significantly higher in PMF compared with ET and PV patients. Furthermore, in vitro assays demonstrated that SPP1 promotes fibroblasts and mesenchymal stromal cells proliferation and collagen production. Strikingly, clinical correlation analyses uncovered that higher SPP1 plasma levels in PMF patients correlate with a more severe fibrosis degree and a shorter overall survival. Collectively our data unveil that MAF overexpression contributes to PMF pathogenesis by driving the deranged production of the profibrotic mediator SPP1.

Published
2018
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