An Automated Cartridge-Based Microfluidic System for Real-Time Quantification of BCR::ABL1 Transcripts in Chronic Myeloid Leukemia: An Italian Experience Alice Costanza Danzero, Enrico Marco Gottardi, Fabrizio Quarantelli, Ciro Del Prete, Alessandra Potenza, Claudia Venturi, Paola Berchialla, Francesca Guerrini, Clara Bono, Emanuela Ottaviani, Sara Galimberti, Carmen Fava, Barbara Izzo International Journal of Molecular Sciences, 2025 Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder caused by the BCR::ABL1 fusion gene, resulting from a reciprocal translocation between chromosomes 22 and 9. Quantification of BCR::ABL1 transcript levels in peripheral blood by RT-qPCR represents the gold standard for molecular response (MR) monitoring, providing essential clinical information on treatment efficacy. Xpert® BCR-ABL Ultra is a fully automated in vitro diagnostic test that quantitatively detects e13a2 and e14a2 BCR::ABL1 transcripts using a single-use cartridge that integrates RNA extraction, cDNA synthesis, nested real-time PCR, and signal detection within a rapid, closed, and user-friendly system. In this study, we evaluated Xpert® BCR-ABL Ultra as an alternative to validated systems currently used by four highly specialized Italian laboratories affiliated with the Italian national laboratory network for CML. A total of 129 peripheral blood samples from CML patients at various disease stages, along with two external quality control materials, were analyzed. We assessed the test’s repeatability, specificity, and stability. Concordance of BCR::ABL1%IS values generated by the different methods was evaluated using EUTOS criteria and Bland–Altman analysis. Finally, MR value concordance was analyzed based on European LeukemiaNet recommendations or calculated using the formula 2 − log10(BCR::ABL1%IS). Xpert® BCR-ABL Ultra demonstrated high repeatability and stability. The BCR::ABL1%IS values obtained with this assay showed strong concordance with those generated by local reference methods, and MR classifications were consistent across platforms. These findings confirm the robustness, accuracy, and efficiency of the Xpert® BCR-ABL Ultra assay, supporting its use as a reliable alternative to currently validated systems for the routine clinical monitoring of CML patients.
Validation Study of Analytical Methods for Multiparameter Flow Cytometry-Based Measurable Residual Disease Assessment in Acute Myeloid Leukemia Martina Barone, Agnese Patuelli, Michele Dicataldo, Maria Irno Consalvo, Gabriella Chirumbolo, Lorenza Bandini, Giulia Atzeni, Dorian Forte, Gianluca Cristiano, Emanuela Ottaviani, Antonio Curti, Francesco Buccisano, Lucia Catani, Mario Arpinati International Journal of Molecular Sciences, 2025 The standardization of multiparameter flow cytometry-based measurable residual disease (MFC-MRD) assessment in acute myeloid leukemia (AML) lacks clear criteria to define leukemia-associated immunophenotypes (LAIPs). In addition, the most specific/sensitive aberrations used to define LAIPs are often partially expressed by the leukemic clone at diagnosis, raising questions about their reliability for accurate MRD quantification. To address this, we investigated whether the quantification of LAIP+ cells reflects residual disease in cases of partial LAIP expression. The following two MFC-MRD approaches were evaluated by comparing their results to RT-qPCR for NPM1 mutations: (1) the LAIP-method, wherein all cells within the patient-specific template created at diagnosis are counted without further gating; (2) the LAIP-based different-from-normal (DfN)-method, wherein cells+ for LAIP-specific aberrant markers are further selected. A total of 125 bone marrow samples from 25 NPM1-mutated AML patients were studied. Our data demonstrate that the LAIP-based DfN-method improves the MFC-MRD accuracy and comparability with molecular MRD. ROC analysis identified cut-offs of 0.034% and 0.095% to discriminate positive/negative results in patients receiving intensive chemotherapy and hypomethylating agents, respectively. We also found distinct accuracy degrees based on the LAIP-specific aberrant markers used for MRD assessment. These results refine the MFC-MRD method and highlight the importance of therapy-specific MRD cut-offs and LAIP classification based on specificity and sensitivity.
Upfront intensive treatment analysis of the Italian Cohort Study on FLT3-mutated AML patients (FLAM): The impact of a FLT3 inhibitor addition to standard chemotherapy in the real-life setting Jacopo Nanni, Irene Azzali, Cristina Papayannidis, Antonino Mulè, Ernesta Audisio, Maria Paola Martelli, Barbara Scappini, Patrizia Chiusolo, Benedetta Cambò, Anna Candoni, Monia Lunghi, Francesco Albano, Attilio Olivieri, Nicola Fracchiolla, Massimo Bernardi, Claudio Romani, Gian Matteo Rigolin, Maria Benedetta Giannini, Monica Bocchia, Elisabetta Todisco, Daniela Cilloni, Maria Teresa Bochicchio, Emanuela Ottaviani, Agnese Mattei, Federica Zamagni, Irene Valli, Roberta Volpi, Giovanni Marconi, Elisabetta Petracci,, Giovanni Martinelli Cancer, 2025 BackgroundThe addition of a FLT3 inhibitor (FLT3i) to standard chemotherapy to treat fit newly diagnosed (ND) patients with FLT3‐mutated acute myeloid leukemia (AML) represents the standard of care resulting from clinical trial results. However, evidence regarding FLT3i adoption in routine clinical practice is still scarce.MethodsClinical data are reported from 394 ND patients with FLT3‐mutated AML enrolled in the retrospective observational Italian Cohort Study on FLT3‐mutated patients with AML and treated with an upfront intensive regimen with (FLT3i group, n = 92) or without (CT group, n = 302) the addition of a FLT3i.ResultsWith a median follow‐up time of 34.5 months, an effectiveness benefit obtained by FLT3i incorporation both in terms of overall survival (median, 34.9 in the FLT3i vs 12.7 months in the CT group, p < .01) and relapse‐free survival (median, 18.9 in the FLT3i vs 7.6 months in the CT group, p = .01) was documented, with a higher composite complete remission rate (75.4% in the FLT3i vs 62.4% in the CT group, p = .052). FLT3i benefit seemed to be independent from the transplant rate.ConclusionsIn conclusion, the benefit of FLT3i addition to upfront intensive treatment in newly diagnosed FLT3‐mutated AML patients was confirmed in a large, real‐life cohort study.
Emergence and Cytogenetic Clonal Evolution of Chromosome 7 Abnormalities in Myeloid Malignancies: Investigating the Role of Telomere Dysfunction Carmen Baldazzi, Lorenza Bandini, Valentina Robustelli, Agnese Patuelli, Claudia Venturi, Alessandra Grassi, Giulia Marzocchi, Angela Ielpo, Vincenza Solli, Maria Teresa Bochicchio, Stefania Paolini, Chiara Sartor, Federico Zingarelli, Antonio Curti, Emanuela Ottaviani, Nicoletta Testoni International Journal of Molecular Sciences, 2025 Monosomy 7 and deletion 7q are common chromosomal abnormalities in myeloid malignancies, and they are associated with a poor prognosis. The mechanism underlying their acquisition remains elusive. We identified a cohort of 24 patients exhibiting clones with different chromosome 7 abnormalities, such as deletion 7q, unstable derivatives (ring chromosomes or ‘naked’ centromeres), and monosomy 7. We designated this group as having cytogenetic clonal evolution of chromosome 7 abnormalities (CCE7). In some cases, CCE7 correlated with disease progression, suggesting that deletions or other derivatives involving the q-arm of chromosome 7 may arise early in the disease course. These abnormalities may be transient but can potentially evolve into monosomy 7. Within the CCE7 group, telomere loss or shortening may contribute to chromosomal instability and the emergence of unstable derivatives, as the chromosome 7 derivatives displayed loss or rearrangement of subtelomeric regions. Moreover, we identified variants in genes implicated in telomere biology disorders and observed specific genetic mutation profiles associated with different chromosome 7 abnormalities. These findings shed light on a potential mechanism leading to monosomy 7 through the evolution of chromosome 7q abnormalities. Identifying patients at risk of developing monosomy 7, based on the presence of unstable derivatives with telomere loss or a specific mutation profile, could potentially enhance patient management and guide the development of novel therapeutic strategies.
Tracking Response and Resistance in Acute Myeloid Leukemia through Single-Cell DNA Sequencing Helps Uncover New Therapeutic Targets Samantha Bruno, Enrica Borsi, Agnese Patuelli, Lorenza Bandini, Manuela Mancini, Dorian Forte, Jacopo Nanni, Martina Barone, Alessandra Grassi, Gianluca Cristiano, Claudia Venturi, Valentina Robustelli, Giulia Atzeni, Cristina Mosca, Sara De Santis, Cecilia Monaldi, Andrea Poletti, Carolina Terragna, Antonio Curti, Michele Cavo, Simona Soverini, Emanuela Ottaviani International Journal of Molecular Sciences, 2024 Acute myeloid leukemia (AML) is an aggressive hematologic neoplasia with a complex polyclonal architecture. Among driver lesions, those involving the FLT3 gene represent the most frequent mutations identified at diagnosis. The development of tyrosine kinase inhibitors (TKIs) has improved the clinical outcomes of FLT3-mutated patients (Pt). However, overcoming resistance to these drugs remains a challenge. To unravel the molecular mechanisms underlying therapy resistance and clonal selection, we conducted a longitudinal analysis using a single-cell DNA sequencing approach (MissionBioTapestri® platform, San Francisco, CA, USA) in two patients with FLT3-mutated AML. To this end, samples were collected at the time of diagnosis, during TKI therapy, and at relapse or complete remission. For Pt #1, disease resistance was associated with clonal expansion of minor clones, and 2nd line TKI therapy with gilteritinib provided a proliferative advantage to the clones carrying NRAS and KIT mutations, thereby responsible for relapse. In Pt #2, clonal architecture was less complex, and 1st line TKI therapy with midostaurin was able to eradicate the leukemic clones. Our results corroborate previous findings about clonal selection driven by TKIs, highlighting the importance of a deeper characterization of individual clonal architectures for choosing the best treatment plan for personalized approaches aimed at optimizing outcomes.
Real-life use of ropeg-interferon α2b in polycythemia vera: patient selection and clinical outcomes Francesca Palandri, F. Branzanti, M. Venturi, A. Dedola, G. Fontana, M. Loffredo, A. Patuelli, E. Ottaviani, M. Bersani, M. Reta, O. Addimanda, V. Vicennati, N. Vianelli, M. Cavo Annals of Hematology, 2024 Ropeginterferon-alfa2b (ropegIFNα2b) is a long-acting IFN formulation with broad FDA/EMA approval as a therapy of polycythemia vera (PV) with no symptomatic splenomegaly. There is currently lack of information on the real-world patient selection, including the impact of local reimbursement policies, and drug management, particularly: type/timing of screening and follow-up tests; absolute/relative contraindications to therapy; ropegIFNα2b dose and combinations with hydroxyurea. As a sub-analysis of the PV-ARC retrospective study (NCT06134102), we here report our monocenter experience with ropegIFNα2b in the period from January 2021, corresponding to drug availability outside clinical trial, and December 2023. Among the 149 patients with EMA/FDA indication, only 55 (36.9%) met the local reimbursement criteria and 18 (12.1%) received ropegIFNα2b. Thanks to appropriate screening, relative/absolute contraindications to ropegIFNα2b were detected and managed in a multidisciplinary manner. Efficacy and safety of ropegIFNα2b was confirmed, with 3 cases of early molecular response. General use of low ropegIFNα2b dose, with frequent need for hydroxyurea combinations, was noted. This real-world experience suggests a significant impact of local regulations on drug prescription and the need for greater real-world data collection on ropegIFNα2b in PV patients. Also, it describes appropriate multidisciplinary screening and monitoring procedures during ropegIFNα2b therapy.
Ex vivo characterization of acute myeloid leukemia patients undergoing hypomethylating agents and venetoclax regimen reveals a venetoclax-specific effect on non-suppressive regulatory T cells and bona fide PD-1+TIM3+ exhausted CD8+ T cells Giulia Corradi, Dorian Forte, Gianluca Cristiano, Andrea Polimeno, Marilena Ciciarello, Valentina Salvestrini, Lorenza Bandini, Valentina Robustelli, Emanuela Ottaviani, Michele Cavo, Darina Ocadlikova, Antonio Curti Frontiers in Immunology, 2024 Acute myeloid leukemia (AML) is an aggressive heterogeneous disease characterized by several alterations of the immune system prompting disease progression and treatment response. The therapies available for AML can affect lymphocyte function, limiting the efficacy of immunotherapy while hindering leukemia-specific immune reactions. Recently, the treatment based on Venetoclax (VEN), a specific B-cell lymphoma 2 (BCL-2) inhibitor, in combination with hypomethylating agents (HMAs) or low-dose cytarabine, has emerged as a promising clinical strategy in AML. To better understand the immunological effect of VEN treatment, we characterized the phenotype and immune checkpoint (IC) receptors’ expression on CD4+ and CD8+ T cells from AML patients after the first and second cycle of HMA in combination with VEN. HMA and VEN treatment significantly increased the percentage of naïve CD8+ T cells and TIM-3+ CD4+ and CD8+ T cells and reduced cytokine-secreting non-suppressive T regulatory cells (Tregs). Of note, a comparison between AML patients treated with HMA only and HMA in combination with VEN revealed the specific contribution of VEN in modulating the immune cell repertoire. Indeed, the reduction of cytokine-secreting non-suppressive Tregs, the increased TIM-3 expression on CD8+ T cells, and the reduced co-expression of PD-1 and TIM-3 on both CD4+ and CD8+ T cells are all VEN-specific. Collectively, our study shed light on immune modulation induced by VEN treatment, providing the rationale for a novel therapeutic combination of VEN and IC inhibitors in AML patients.
A venetoclax and azacitidine bridge-to-transplant strategy for NPM1-mutated acute myeloid leukaemia in molecular failure C. Sartor, L. Brunetti, E. Audisio, A. Cignetti, L. Zannoni, G. Cristiano, J. Nanni, R. Ciruolo, F. Zingarelli, E. Ottaviani, A. Patuelli, L. Bandini, D. Forte, S. Sciabolacci, V. Cardinali, C. Papayannidis, M. Cavo, M. P. Martelli, A. Curti British Journal of Haematology, 2023 NPM1-mutated acute myeloid leukaemia (NPM1mut AML) represents a mostly favourable/intermediate risk disease that benefits from allogeneic haematopoietic stem cell transplantation (HSCT) in case of measurable residual disease (MRD) relapse or persistence after induction chemotherapy. Although the negative prognostic role of pre-HSCT MRD is established, no recommendations are available for the management of peri-transplant molecular failure (MF). Based on the efficacy data of venetoclax (VEN)-based treatment in NPM1mut AML older patients, we retrospectively analysed the off-label combination of VEN plus azacitidine (AZA) as bridge-to-transplant strategy in 11 NPM1mut MRD-positive fit AML patients. Patients were in MRD-positive complete remission (CRMRDpos ) at the time of treatment: nine in molecular relapse and two in molecular persistence. After a median number of two cycles (range 1-4) of VEN-AZA, 9/11 (81.8%) achieved CRMRD -negative (CRMRDneg ). All 11 patients proceeded to HSCT. With a median follow-up from treatment start of 26 months, and a median post-HSCT follow-up of 19 months, 10/11 patients are alive (1 died from non-relapse mortality), and 9/10 patients are in MRDneg status. This patient series highlights the efficacy and safety of VEN-AZA to prevent overt relapse, achieve deep responses and preserve patient fitness before HSCT, in patients with NPM1mut AML in MF.
Prognosis in Chronic Myeloid Leukemia: Baseline Factors, Dynamic Risk Assessment and Novel Insights Miriam Iezza, Sofia Cortesi, Emanuela Ottaviani, Manuela Mancini, Claudia Venturi, Cecilia Monaldi, Sara De Santis, Nicoletta Testoni, Simona Soverini, Gianantonio Rosti, Michele Cavo, Fausto Castagnetti Cells, 2023 The introduction of tyrosine kinase inhibitors (TKIs) has changed the treatment paradigm of chronic myeloid leukemia (CML), leading to a dramatic improvement of the outcome of CML patients, who now have a nearly normal life expectancy and, in some selected cases, the possibility of aiming for the more ambitious goal of treatment-free remission (TFR). However, the minority of patients who fail treatment and progress from chronic phase (CP) to accelerated phase (AP) and blast phase (BP) still have a relatively poor prognosis. The identification of predictive elements enabling a prompt recognition of patients at higher risk of progression still remains among the priorities in the field of CML management. Currently, the baseline risk is assessed using simple clinical and hematologic parameters, other than evaluating the presence of additional chromosomal abnormalities (ACAs), especially those at “high-risk”. Beyond the onset, a re-evaluation of the risk status is mandatory, monitoring the response to TKI treatment. Moreover, novel critical insights are emerging into the role of genomic factors, present at diagnosis or evolving on therapy. This review presents the current knowledge regarding prognostic factors in CML and their potential role for an improved risk classification and a subsequent enhancement of therapeutic decisions and disease management.
Release of IFNg by Acute Myeloid Leukemia Cells Remodels Bone Marrow Immune Microenvironment by Inducing Regulatory T Cells Giulia Corradi, Barbara Bassani, Giorgia Simonetti, Sabina Sangaletti, Jayakumar Vadakekolathu, Maria Chiara Fontana, Martina Pazzaglia, Alessandro Gulino, Claudio Tripodo, Gianluca Cristiano, Lorenza Bandini, Emanuela Ottaviani, Darina Ocadlikova, Milena Piccioli, Giovanni Martinelli, Mario Paolo Colombo, Sergio Rutella, Michele Cavo, Marilena Ciciarello, Antonio Curti Clinical Cancer Research, 2022
Peripheral blasts are associated with responses to ruxolitinib and outcomes in patients with chronic-phase myelofibrosis Francesca Palandri, Daniela Bartoletti, Alessandra Iurlo, Massimiliano Bonifacio, Elisabetta Abruzzese, Giovanni Caocci, Elena M. Elli, Giuseppe Auteri, Mario Tiribelli, Nicola Polverelli, Maurizio Miglino, Florian H. Heidel, Alessia Tieghi, Giulia Benevolo, Eloise Beggiato, Carmen Fava, Francesco Cavazzini, Novella Pugliese, Gianni Binotto, Costanza Bosi, Bruno Martino, Monica Crugnola, Emanuela Ottaviani, Giorgia Micucci, Malgorzata M. Trawinska, Antonio Cuneo, Monica Bocchia, Mauro Krampera, Fabrizio Pane, Roberto M. Lemoli, Daniela Cilloni, Nicola Vianelli, Michele Cavo, Giuseppe A. Palumbo, Massimo Breccia Cancer, 2022
Droplet digital pcr for bcr–abl1 monitoring in diagnostic routine: Ready to start? Maria Teresa Bochicchio, Jessica Petiti, Paola Berchialla, Barbara Izzo, Emilia Giugliano, Emanuela Ottaviani, Santa Errichiello, Giovanna Rege-Cambrin, Claudia Venturi, Luigiana Luciano, Filomena Daraio, Daniele Calistri, Gianantonio Rosti, Giuseppe Saglio, Giovanni Martinelli, Fabrizio Pane, Daniela Cilloni, Enrico M. Gottardi, Carmen Fava Cancers, 2021
Integrated genomic-metabolic classification of acute myeloid leukemia defines a subgroup with NPM1 and cohesin/DNA damage mutations Giorgia Simonetti, Carlo Mengucci, Antonella Padella, Eugenio Fonzi, Gianfranco Picone, Claudio Delpino, Jacopo Nanni, Rossella De Tommaso, Eugenia Franchini, Cristina Papayannidis, Giovanni Marconi, Martina Pazzaglia, Margherita Perricone, Emanuela Scarpi, Maria Chiara Fontana, Samantha Bruno, Michela Tebaldi, Anna Ferrari, Maria Teresa Bochicchio, Andrea Ghelli Luserna Di Rorà, Martina Ghetti, Roberta Napolitano, Annalisa Astolfi, Carmen Baldazzi, Viviana Guadagnuolo, Emanuela Ottaviani, Ilaria Iacobucci, Michele Cavo, Gastone Castellani, Torsten Haferlach, Daniel Remondini, Francesco Capozzi, Giovanni Martinelli Leukemia, 2021
Case Report: A Novel Activating FLT3 Mutation in Acute Myeloid Leukemia Samantha Bruno, Lorenza Bandini, Agnese Patuelli, Valentina Robustelli, Claudia Venturi, Manuela Mancini, Dorian Forte, Sara De Santis, Cecilia Monaldi, Alessandra Grassi, Gabriella Chiurumbolo, Stefania Paolini, Gianluca Cristiano, Cristina Papayannidis, Chiara Sartor, Jacopo Nanni, Emanuela Ottaviani, Antonio Curti, Michele Cavo, Simona Soverini Frontiers in Oncology, 2021
MEC (mitoxantrone, etoposide, and cytarabine) induces complete remission and is an effective bridge to transplant in acute myeloid leukemia Giovanni Marconi, Annalisa Talami, Maria Chiara Abbenante, Chiara Sartor, Sarah Parisi, Jacopo Nanni, Luca Bertamini, Simone Ragaini, Matteo Olivi, Stefano de Polo, Gianluca Cristiano, Maria Chiara Fontana, Maria Teresa Bochicchio, Emanuela Ottaviani, Mario Arpinati, Mariarosaria Sessa, Carmen Baldazzi, Lucia Caso, Nicoletta Testoni, Michele Baccarani, Francesca Bonifazi, Giovanni Martinelli, Stefania Paolini, Michele Cavo, Cristina Papayannidis, Antonio Curti European Journal of Haematology, 2020
Novel and rare fusion transcripts involving transcription factors and tumor suppressor genes in acute myeloid leukemia Antonella Padella, Giorgia Simonetti, Giulia Paciello, George Giotopoulos, Carmen Baldazzi, Simona Righi, Martina Ghetti, Anna Stengel, Viviana Guadagnuolo, Rossella De Tommaso, Cristina Papayannidis, Valentina Robustelli, Eugenia Franchini, Andrea Ghelli Luserna di Rorà, Anna Ferrari, Maria Chiara Fontana, Samantha Bruno, Emanuela Ottaviani, Simona Soverini, Clelia Tiziana Storlazzi, Claudia Haferlach, Elena Sabattini, Nicoletta Testoni, Ilaria Iacobucci, Brian J. P. Huntly, Elisa Ficarra, Giovanni Martinelli Cancers, 2019
Aneuploid acute myeloid leukemia exhibits a signature of genomic alterations in the cell cycle and protein degradation machinery Giorgia Simonetti, Antonella Padella, Italo Farìa do Valle, Maria Chiara Fontana, Eugenio Fonzi, Samantha Bruno, Carmen Baldazzi, Viviana Guadagnuolo, Marco Manfrini, Anna Ferrari, Stefania Paolini, Cristina Papayannidis, Giovanni Marconi, Eugenia Franchini, Elisa Zuffa, Maria Antonella Laginestra, Federica Zanotti, Annalisa Astolfi, Ilaria Iacobucci, Simona Bernardi, Marco Sazzini, Elisa Ficarra, Jesus Maria Hernandez, Peter Vandenberghe, Jan Cools, Lars Bullinger, Emanuela Ottaviani, Nicoletta Testoni, Michele Cavo, Torsten Haferlach, Gastone Castellani, Daniel Remondini, Giovanni Martinelli Cancer, 2019
Identification of Two DNMT3A Mutations Compromising Protein Stability and Methylation Capacity in Acute Myeloid Leukemia Samantha Bruno, Maria Teresa Bochicchio, Eugenia Franchini, Antonella Padella, Giovanni Marconi, Andrea Ghelli Luserna di Rorà, Claudia Venturi, Maddalena Raffini, Giovanna Prisinzano, Anna Ferrari, Lorenza Bandini, Valentina Robustelli, Martina Pazzaglia, Maria Chiara Fontana, Chiara Sartor, Maria Chiara Abbenante, Cristina Papayannidis, Simona Soverini, Emanuela Ottaviani, Giorgia Simonetti, Giovanni Martinelli Journal of Oncology, 2019
Chromothripsis in acute myeloid leukemia: Biological features and impact on survival Maria Chiara Fontana, Giovanni Marconi, Jelena D. Milosevic Feenstra, Eugenio Fonzi, Cristina Papayannidis, Andrea Ghelli Luserna di Rorá, Antonella Padella, Vincenza Solli, Eugenia Franchini, Emanuela Ottaviani, Anna Ferrari, Carmen Baldazzi, Nicoletta Testoni, Ilaria Iacobucci, Simona Soverini, Torsten Haferlach, Viviana Guadagnuolo, Lukas Semerad, Michael Doubek, Michael Steurer, Zdenek Racil, Stefania Paolini, Marco Manfrini, Michele Cavo, Giorgia Simonetti, Robert Kralovics, Giovanni Martinelli Leukemia, 2018
In vitro and in vivo single-agent efficacy of checkpoint kinase inhibition in acute lymphoblastic leukemia Ilaria Iacobucci, Andrea Ghelli Luserna Di Rorà, Maria Vittoria Verga Falzacappa, Claudio Agostinelli, Enrico Derenzini, Anna Ferrari, Cristina Papayannidis, Annalisa Lonetti, Simona Righi, Enrica Imbrogno, Silvia Pomella, Claudia Venturi, Viviana Guadagnuolo, Federica Cattina, Emanuela Ottaviani, Maria Chiara Abbenante, Antonella Vitale, Loredana Elia, Domenico Russo, Pier Luigi Zinzani, Stefano Pileri, Pier Giuseppe Pelicci, Giovanni Martinelli Journal of Hematology and Oncology, 2015
NPM1 mutations may reveal acute myeloid leukemia in cases otherwise morphologically diagnosed as myelodysplastic syndromes or myelodysplastic/myeloproliferative neoplasms Fabio Forghieri, Ambra Paolini, Monica Morselli, Sara Bigliardi, Goretta Bonacorsi, Giovanna Leonardi, Valeria Coluccio, Monica Maccaferri, Valeria Fantuzzi, Laura Faglioni, Elisabetta Colaci, Francesco Soci, Vincenzo Nasillo, Andrea Messerotti, Laura Arletti, Valeria Pioli, Patrizia Zucchini, Chiara Quadrelli, Giorgia Corradini, Francesca Giacobbi, Daniela Vallerini, Giovanni Riva, Patrizia Barozzi, Ivana Lagreca, Roberto Marasca, Franco Narni, Cristina Mecucci, Emanuela Ottaviani, Giovanni Martinelli, Brunangelo Falini, Mario Luppi, Leonardo Potenza Leukemia and Lymphoma, 2015
A case report of acute myeloid leukemia and neurofibromatosis 1 Chiara Sartor, Cristina Papayannidis, Maria Chiara Abbenante, Antonio Curti, Nicola Polverelli, Emanuela Ottaviani, Ilaria Iacobucci, Viviana Guadagnuolo, Giovanni Martinelli Hematology Reports, 2013
IKAROS deletions dictate a unique gene expression signature in patients with adult B-cell acute lymphoblastic Leukemia Ilaria Iacobucci, Nunzio Iraci, Monica Messina, Annalisa Lonetti, Sabina Chiaretti, Emanuele Valli, Anna Ferrari, Cristina Papayannidis, Francesca Paoloni, Antonella Vitale, Clelia Tiziana Storlazzi, Emanuela Ottaviani, Viviana Guadagnuolo, Sandra Durante, Marco Vignetti, Simona Soverini, Fabrizio Pane, Robin Foà, Michele Baccarani, Markus Müschen, Giovanni Perini, Giovanni Martinelli Plos One, 2012
The molecular anatomy of the FIP1L1-PDGFRA fusion gene C Walz, J Score, J Mix, D Cilloni, C Roche-Lestienne, R-F Yeh, J L Wiemels, E Ottaviani, P Erben, A Hochhaus, M Baccarani, D Grimwade, C Preudhomme, J Apperley, G Martinelli, G Saglio, N C P Cross, A Reiter, on behalf of the European LeukemiaNet Leukemia, 2009
A case of coexistence between JAK2V617F and BCR/ABL Simonetta Pardini, Claudio Fozza, Salvatore Contini, Elena Rimini, Emanuela Ottaviani, Marilina Amabile, Gianantonio Rosti, Maurizio Longinotti European Journal of Haematology, 2008
Farnesyltransferase inhibition in hematologic malignancies: The clinical experience with tipifarnib Clinical Advances in Hematology and Oncology, 2008
Case-control study of multidrug resistance phenotype and response to induction treatment including or not fludarabine in newly diagnosed acute myeloid leukaemia patients Michele Malagola, Daniela Damiani, Giovanni Martinelli, Angela Michelutti, Bruno Cesana, Antonio De Vivo, Pier Paolo Piccaluga, Emanuela Ottaviani, Anna Candoni, Antonella Geromin, Mario Tiribelli, Renato Fanin, Nicoletta Testoni, Francesco Lauria, Monica Bocchia, Marco Gobbi, Ivana Pierri, Alfonso Zaccaria, Eliana Zuffa, Patrizio Mazza, Giancarla Priccolo, Luigi Gugliotta, Alessandro Bonini, Giuseppe Visani, Cristina Skert, Cesare Bergonzi, Aldo Maria Roccaro, Carla Filí, Michele Baccarani, Domenico Russo British Journal of Haematology, 2007
Imatinib mesylate in the treatment of c-kit-positive acute myeloid leukemia: Is this the real target? [3] (multiple letters) Michele Malagola, Giovanni Martinelli, Michela Rondoni, Stefania Paolini, Stavrula Gaitani, Mario Arpinati, Pier Paolo Piccaluga, Marilina Amabile, Constanza Basi, Emanuela Ottaviani, Anna Candoni, Enrico Gottardi, Daniela Cilloni, Monica Bocchia, Giuseppe Saglio, Francesco Lauria, Renato Fanin, Giuseppe Visani, Maria Carla Marrè, Michela Maderna, Francesca Rancati, Vincenza Vinaccia, Domenico Russo, Michele Baccarani Blood, 2005
Molecular monitoring to identify a threshold of CBFβ/MYH11 transcript below which continuous complete remission of acute myeloid leukemia inv(16) is likely Haematologica, 2004
Imatinib mesylate can induce complete molecular remission in FIP1L1-PDGFR-α positive idiopathic hypereosinophilic syndrome Haematologica, 2004
Two more inv(16) acute myeloid leukemia cases with infrequent CBFβ-MYH11 fusion transcript: Clinical and molecular findings [4] Haematologica, 2002
Novel types of bcr-abl transcript with breakpoints in BCR exon 8 found in Philadelphia-positive patients with typical chronic myeloid leukemia retain the sequence encoding for the DBL- and CDC24-homology domains but not the pleckstrin homology one Haematologica, 2002
Clonal eosinophils are a morphologic hallmark of ETV6/ABL1 positive acute myeloid leukemia Haematologica, 2002
Molecular therapy for multiple myeloma Haematologica, 2001
Real-time quantification of different types of bcr-abl transcript in chronic myeloid leukemia Haematologica, 2001
Polymerase chain reaction-based detection of minimal residual disease in multiple myeloma patients receiving allogeneic stem cell transplantation Haematologica, 2000
Clinical value of quantitative long-term assessment of bcr-abl chimeric transcript in chronic myelogenous leukemia patients after allogeneic bone marrow transplantation Haematologica, 2000
Long-term disease-free acute myeloblastic leukemia with inv(16) is associated with PCR undetectable CBFβ/MYH11 transcript Haematologica, 2000
Alu and translisin recognition site sequences flanking translocation sites in a novel type of chimeric bcr-abl transcript suggest a possible general mechanism for bcr-abl breakpoints Haematologica, 2000
Clinical and molecular follow-up by amplification of the CDR-III IgH region in multiple myeloma patients after autologous transplantation of hematopoietic CD34+ stem cells Haematologica, 1999
3q21 and 3q26 cytogenetic abnormalities in acute myeloblastic leukemia: Biological and clinical features Haematologica, 1999
Role of autologous bone marrow transplantation as consolidation chemotherapy in acute promyelocytic leukemia patients in complete remission Haematologica, 1998
Long-term disease-free acute promyelocytic leukemia patients really can be cured at molecular level Haematologica, 1998
Disappearance of PML/RARα acute promyelocytic leukemia-associated transcript during consolidation chemotherapy Haematologica, 1998
Detection of bcr-abl transcript in chronic myelogenous leukemia patients by reverse-transcription-polymerase chain reaction and capillary electrophoresis Haematologica, 1998
Adenoviral mediated gene transfer can be accomplished in human myeloid cell lines and is inhibited by all-trans retinoic acid-induced differentiation Haematologica, 1997
The expression of proliferation and quiescence associated antigens in acute myeloid leukemia correlates with survival duration: Analysis of 15 refractory cases Haematologica, 1997
All-trans retionic ACid in the treatment of myelodysplastic syndromes G. Visani, P. Tosi, S. Manfroi, E. Ottaviani, C. Finelli, A. Cenacchi, M. Bendandi, S. Tura, Mashiro Imamura, Masharu Kasai, Xiaofan Zhu, Sumiko Kobayashi, Satoshi Hashino, Toshio Higa, Keisuke Sakurada, Masahiro Asaka Leukemia and Lymphoma, 1995
Serum levels of granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in treated patients with chronic myelogenous leukemia in chronic phase Haematologica, 1994
Fludarabine + ARA-C + G-CSF: Cytotoxic effect and induction of apoptosis on fresh acute myeloid leukemia cells Leukemia, 1994
All-trans retinoic acid potentiates megakaryocyte colony formation: In vitro and in vivo effects after administration to acute promyelocytic leukemia patients Leukemia, 1994
FLAG (fludarabine + high-dose cytarabine + G-CSF): An effective and tolerable protocol for the treatment of 'poor risk' acute myeloid leukemias Leukemia, 1994
