10 results on '"Spadano, R."'
Search Results
2. Managing chronic myeloid leukemia for treatment-free remission: A proposal from the GIMEMA CML WP
- Author
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Francesca Lunghi, Gabriele Gugliotta, Chiara Elena, Valentina Giai, Monica Bocchia, Marco Cerrano, Monia Lunghi, Gaetano La Barba, Fausto Castagnetti, Germana Beltrami, Simona Soverini, Paola Fazi, Micaela Bergamaschi, Sara Galimberti, Mario Tiribelli, Claudio Fozza, Antonella Gozzini, Fabrizio Pane, Elena Trabacchi, Massimo Breccia, Mario Annunziata, Isabella Capodanno, Domenico Russo, Serena Rupoli, Sara Barulli, Giovanna Rege-Cambrin, Michele Baccarani, Gianni Binotto, Fausto Palmieri, Roberto Marasca, Bruno Martino, Alessandro Lucchesi, E Abruzzese, Paolo Vigneri, Carmen Fava, Alessandra Iurlo, Francesco Albano, Caterina Musolino, Michele Cedrone, Luigia Luciano, Fabio Stagno, Gianantonio Rosti, Patrizia Pregno, Rosaria Sancetta, Angela Melpignano, Raffaele Spadano, Massimiliano Bonifacio, Luciano Levato, Marzia Salvucci, Vincenzo Accurso, Monica Crugnola, Michele Malagola, Davide Rapezzi, Giovanni Caocci, Mariella D'Adda, Simona Sica, Giuseppe Saglio, Maria Cristina Miggiano, Enrico Montefusco, Simona Tomassetti, Francesco Cavazzini, Baccarani, M., Abruzzese, E., Accurso, V., Albano, F., Annunziata, M., Barulli, S., Beltrami, G., Bergamaschi, M., Binotto, G., Bocchia, M., Caocci, G., Capodanno, I., Cavazzini, F., Cedrone, M., Cerrano, M., Crugnola, M., D'Adda, M., Elena, C., Fava, C., Fazi, P., Fozza, C., Galimberti, S., Giai, V., Gozzini, A., Gugliotta, G., Iurlo, A., la Barba, G., Levato, L., Lucchesi, A., Luciano, L., Lunghi, F., Lunghi, M., Malagola, M., Marasca, R., Martino, B., Melpignano, A., Miggiano, M. C., Montefusco, E., Musolino, C., Palmieri, F., Pregno, P., Rapezzi, D., Rege-Cambrin, G., Rupoli, S., Salvucci, M., Sancetta, R., Sica, S., Spadano, R., Stagno, F., Tiribelli, M., Tomassetti, S., Trabacchi, E., Bonifacio, M., Breccia, M., Castagnetti, F., Pane, F., Russo, D., Saglio, G., Soverini, S., Vigneri, P., Rosti, G., Baccarani M., Abruzzese E., Accurso V., Albano F., Annunziata M., Barulli S., Beltrami G., Bergamaschi M., Binotto G., Bocchia M., Caocci G., Capodanno I., Cavazzini F., Cedrone M., Cerrano M., Crugnola M., D'Adda M., Elena C., Fava C., Fazi P., Fozza C., Galimberti S., Giai V., Gozzini A., Gugliotta G., Iurlo A., la Barba G., Levato L., Lucchesi A., Luciano L., Lunghi F., Lunghi M., Malagola M., Marasca R., Martino B., Melpignano A., Miggiano M.C., Montefusco E., Musolino C., Palmieri F., Pregno P., Rapezzi D., Rege-Cambrin G., Rupoli S., Salvucci M., Sancetta R., Sica S., Spadano R., Stagno F., Tiribelli M., Tomassetti S., Trabacchi E., Bonifacio M., Breccia M., Castagnetti F., Pane F., Russo D., Saglio G., Soverini S., Vigneri P., and Rosti G.
- Subjects
Male ,Pediatrics ,Fusion Proteins, bcr-abl ,Chronic myelogenous leukemia ,tyrosine kinase inhibitors ,additional chromosomal-abnormalities ,deep molecular responses ,high-dose imatinib ,randomized cml ,domain mutations ,prognostic-significance ,cytogenetic response ,frontline nilotinib ,Pregnancy ,chronic myeloid leukemia,management,recommendations,Gimema,treatment-free remission ,hemic and lymphatic diseases ,Antineoplastic Combined Chemotherapy Protocols ,Medicine ,Young adult ,Disease management (health) ,Myeloid Neoplasia ,Remission Induction ,Myeloid leukemia ,Disease Management ,Hematology ,Health Care Costs ,Middle Aged ,Leukemia ,Treatment Outcome ,Italy ,Retreatment ,Treatment strategy ,Female ,management ,Human ,Adult ,medicine.medical_specialty ,Adolescent ,Chronic Myeloid Leukemia ,Protein Kinase Inhibitor ,Socio-culturale ,Treatment-Free Remission ,Gimema ,Myelogenous ,Young Adult ,Leukemia, Myelogenous, Chronic, BCR-ABL Positive ,Long term survival ,Humans ,Protein Kinase Inhibitors ,Antineoplastic Combined Chemotherapy Protocol ,business.industry ,medicine.disease ,Health Care Cost ,Settore MED/15 - MALATTIE DEL SANGUE ,treatment in chronic phase chronic myeloid leukemia ,Health Care Survey ,Health Care Surveys ,recommendations ,Disease risk ,business - Abstract
Several papers authored by international experts have proposed recommendations on the management of BCR-ABL1+ chronic myeloid leukemia (CML). Following these recommendations, survival of CML patients has become very close to normal. The next, ambitious, step is to bring as many patients as possible into a condition of treatment-free remission (TFR). The Gruppo Italiano Malattie EMatologiche dell’Adulto (GIMEMA; Italian Group for Hematologic Diseases of the Adult) CML Working Party (WP) has developed a project aimed at selecting the treatment policies that may increase the probability of TFR, taking into account 4 variables: the need for TFR, the tyrosine kinase inhibitors (TKIs), the characteristics of leukemia, and the patient. A Delphi-like method was used to reach a consensus among the representatives of 50 centers of the CML WP. A consensus was reached on the assessment of disease risk (EUTOS Long Term Survival [ELTS] score), on the definition of the most appropriate age boundaries for the choice of first-line treatment, on the choice of the TKI for first-line treatment, and on the definition of the responses that do not require a change of the TKI (BCR-ABL1 ≤10% at 3 months, ≤1% at 6 months, ≤0.1% at 12 months, ≤0.01% at 24 months), and of the responses that require a change of the TKI, when the goal is TFR (BCR-ABL1 >10% at 3 and 6 months, >1% at 12 months, and >0.1% at 24 months). These suggestions may help optimize the treatment strategy for TFR.
- Published
- 2019
3. Genetic polymorphisms associated with telomere length and risk of developing myeloproliferative neoplasms
- Author
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Aleksandra Gołos, Aleksandra Butrym, José Maldonado, Federico Canzian, Daniele Campa, Francesca Tavano, Francisca Hernández Mohedo, Matteo Giaccherini, Manuel Jurado, Federica Gemignani, Nicola Sgherza, Joanna Gora-Tybor, Joaquin Martinez Lopez, Grzegorz Mazur, Raffaele Spadano, Judit Várkonyi, Andres Jerez, Juan Sainz, Angelica Macauda, [Giaccherini,M, Macauda,A, Gemignani,F, Campa,D] Department of Biology, University of Pisa, Pisa, Italy. [Giaccherini,M, Canzian,F] Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. [Sgherza,N] Division of Hematology, Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy. [Sgherza,N] U.O.C. Ematologia con Trapianto, Azienda Ospedaliero-Universitaria Consorzionale, Policlinico di Bari, Bari, Italy. [Sainz,J, Sanchez Maldonado,JM, Jurado,M] Genomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer / University of Granada / Andalusian Regional Government, PTS Granada, Granada, Spain. [Sainz,J, Jurado,M, Hernández Mohedo,F] Monoclonal Gammopathies Unit, University Hospital Virgen de las Nieves, Granada, Spain. [Sainz,J, Hernández Mohedo,F] Pharmacogenetics Unit, Instituto de Investigación Biosanitaria de Granada (Ibs. Granada), Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. [Sainz,J] Department of Medicine, University of Granada, Granada, Spain. [Tavano,F] Division of Gastroenterology and Research Laboratory, Fondazione IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy. [Mazur,G] Department of Internal Medicine, Occupational Diseases, Hypertension and Clinical Oncology, Wroclaw Medical University, Wroclaw, Poland. [Jerez,A] Hematology and Medical Oncology Department, University Hospital Morales Meseguer-IMIB, CIBERER, Murcia, Spain. [Góra-Tybor,J] Department of Hematology, Medical University of Łódź, Łódź, Poland. [Gołos,A] Department of Clinical Oncology and Chemotherapy, Magodent Hospital, Warsaw, Poland. [Martinez Lopez,J] Hospital 12 de Octubre, H12O-CNIO Hematological Malignancies Clinical Research Unitc Compluntense University, CIBERONC, Madrid, Spain. [Várkonyi,J] Third Department of Internal Medicine, Semmelweis University, Budapest, Hungary. [Spadano,R] Division of Hematology, Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy. [Butrym,A] Department of Cancer Prevention and Therapy, Wroclaw Medical University, Wroclaw, Poland., and This work was partially supported by intramural funds of Univerity of Pisa and DKFZ, and by the Italian Ministry of Health grants to the Division of Gastroenterology, Fondazione IRCCS 'Casa Sollievo della Sofferenza' Hospital, San Giovanni Rotondo (F.G.), Italy and by the '5 × 1000' voluntary contribution.Open access funding provided by Projekt DEA.
- Subjects
Male ,Oncology ,Polimorfismo de nucleótido simple ,Epidemiology ,Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Probability::Risk::Risk Factors [Medical Subject Headings] ,Myeloproliferative neoplasms ,Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings] ,0302 clinical medicine ,Risk Factors ,Neoplasms ,Medicine ,Persons::Persons::Age Groups::Adult::Aged [Medical Subject Headings] ,Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Case-Control Studies [Medical Subject Headings] ,Predisposición genética a la enfermedad ,Hematology ,Telomere ,Diseases::Neoplasms [Medical Subject Headings] ,Middle Aged ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Neoplasias ,030220 oncology & carcinogenesis ,Phenomena and Processes::Genetic Phenomena::Genetic Processes::Cell Division::Telomere Homeostasis [Medical Subject Headings] ,Female ,medicine.medical_specialty ,Check Tags::Male [Medical Subject Headings] ,Single-nucleotide polymorphism ,Case-control studies ,Polymorphism, Single Nucleotide ,lcsh:RC254-282 ,Article ,Diseases::Pathological Conditions, Signs and Symptoms::Pathologic Processes::Disease Attributes::Disease Susceptibility::Genetic Predisposition to Disease [Medical Subject Headings] ,03 medical and health sciences ,Internal medicine ,Humans ,Genetic Predisposition to Disease ,Allele ,Aged ,Diseases::Hemic and Lymphatic Diseases::Hematologic Diseases::Bone Marrow Diseases::Myeloproliferative Disorders [Medical Subject Headings] ,Phenomena and Processes::Genetic Phenomena::Genetic Variation::Polymorphism, Genetic::Polymorphism, Single Nucleotide [Medical Subject Headings] ,Myeloproliferative Disorders ,business.industry ,Telomere Homeostasis ,Cancer ,Persons::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings] ,medicine.disease ,Increased risk ,Check Tags::Female [Medical Subject Headings] ,Risk factors ,Risk allele ,business ,Telómero ,030215 immunology - Abstract
D.C., F.C., and M.G. conceived and designed the study. A.M. and M.G. performed labwork. A.M., F.C., D.C., and M.G. drafted the manuscript. A.M., F.C., D.C., and M.G. performed data quality control and statistical analyses. All other authors provided samples and data. All authors critically read, commented, and approved the manuscript., Telomere length measured in leukocyte (LTL) has been found to be associated with the risk of developing several cancer types, including myeloproliferative neoplasms (MPNs). LTL is genetically determined by, at least, 11 SNPs previously shown to influence LTL. Their combination in a score has been used as a genetic instrument to measure LTL and evaluate the causative association between LTL and the risk of several cancer types. We tested, for the first time, the “teloscore” in 480 MPN patients and 909 healthy controls in a European multi-center case–control study. We found an increased risk to develop MPNs with longer genetically determined telomeres (OR = 1.82, 95% CI 1.24–2.68, P = 2.21 × 10−3, comparing the highest with the lowest quintile of the teloscore distribution). Analyzing the SNPs individually we confirm the association between TERT-rs2736100-C allele and increased risk of developing MPNs and we report a novel association of the OBFC1-rs9420907-C variant with higher MPN risk (ORallelic= 1.43; 95% CI 1.15–1.77; P = 1.35 × 10−3). Consistently with the results obtained with the teloscore, both risk alleles are also associated with longer LTL. In conclusion, our results suggest that genetically determined longer telomeres could be a risk marker for MPN development
- Published
- 2020
4. Survival and late effects of hematopoietic cell transplantation in patients with thalassemia major.
- Author
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Santarone S, Angelini S, Natale A, Vaddinelli D, Spadano R, Casciani P, Papola F, Di Lembo E, Iannetti G, and Di Bartolomeo P
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- Male, Female, Infant, Newborn, Humans, Child, Retrospective Studies, Disease-Free Survival, Disease Progression, Transplantation Conditioning adverse effects, beta-Thalassemia therapy, COVID-19, Hematopoietic Stem Cell Transplantation adverse effects, Neoplasms, Second Primary etiology
- Abstract
In this retrospective study, we evaluated long-term survival and late effects in 137 patients affected by thalassemia major (TM) who received an allogeneic hematopoietic cell transplantation (HCT). Median age at HCT was 10.1 years. After a median follow-up of 30 years, 114 (83.2%) patients are living and 108 (78.8%) are cured. The cumulative incidence of nonrelapse mortality and thalassemia recurrence was 9.5% at 1 year and 10.2% at 39 years respectively. The 39-years cumulative incidence of overall survival and disease-free survival were 81.4% and 74.5%. One hundred twenty-three patients who survived more than 2 years after HCT were evaluated for late effects concerning hematological disorders, iron burden, growth, obesity, diabetes mellitus, thyroid and gonadal function, eye, heart, liver, lung, kidney, gastrointestinal, neurologic and psychiatric system, osteoarticular system, secondary solid cancer (SSC), performance status, and Covid-19 infection. Fertility was preserved in 21 males whose partners delivered 34 neonates and 25 females who delivered 26 neonates. Fifteen cases of SSC were diagnosed for a 39-year cumulative incidence of 16.4%. HCT represents a definitive cure for the majority of TM patients at the price, however, of a non-negligible early and late mortality which in the long run affects survival and disease-free survival., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)
- Published
- 2022
- Full Text
- View/download PDF
5. Log reduction of leukemic cells and minimal residual disease by flow cytometry represent effective predictors of clinical outcome in elderly patients with acute myeloid leukemia.
- Author
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Rossi G, Giambra V, de Waure C, Giacchetta I, Minervini MM, Abbenante MC, Spadano R, La Torre A, Scalzulli PR, and Cascavilla N
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- Aged, Flow Cytometry methods, Hematologic Tests, Humans, Neoplasm, Residual diagnosis, Neoplasm, Residual drug therapy, Neoplasm, Residual genetics, Leukemia, Myeloid, Acute diagnosis, Leukemia, Myeloid, Acute drug therapy, Leukemia, Myeloid, Acute genetics
- Abstract
Background: Nowadays minimal residual disease (MRD) and log-reduction of leukemic cells are poorly investigated in elderly patients with acute myeloid leukemia (AML) treated with hypometilating agents (HMAs). Studies focusing on MRD in elderly AML patients who received HMAs are scant and devoid of rigorous criteria for both enrollment and monitoring. Log-reduction has never been investigated in these patients. Thus, the purpose of our study was to compare the prognostic impact of MRD and log-reduction of leukemic cells at the optimal time of assessment in older AML patients., Methods: Elderly patients who completed at least six cycles of HMAs and showed suitable leukemia-associated immunophenotypes (LAIPs) for the MRD and log-reduction assessment by flow cytometry were enrolled in the study., Results: After comparing the times of assessment C4 (4-cycles) and C6 (6-cycles), C6 has been chosen as optimal. Patients who achieved MRD negativity or 2-log-reduction of leukemic cells at C6 had a significantly longer DFS. Particularly, results of 2-log-reduction were confirmed a multivariate analysis. Patients with MRD negativity or 2-log reduction of leukemic cells showed an improvement of their OS, although not significantly., Conclusions: Our data confirmed the predictive role of MRD and 2-log reduction also in older AML patients treated with HMAs., (© 2021 International Clinical Cytometry Society.)
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- 2022
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6. Do myeloproliferative neoplasms and multiple myeloma share the same genetic susceptibility loci?
- Author
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Macauda A, Giaccherini M, Sainz J, Gemignani F, Sgherza N, Sánchez-Maldonado JM, Gora-Tybor J, Martinez-Lopez J, Carreño-Tarragona G, Jerez A, Spadano R, Gołos A, Jurado M, Hernández-Mohedo F, Mazur G, Tavano F, Butrym A, Várkonyi J, Canzian F, and Campa D
- Subjects
- Aged, Female, Genetic Loci, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Male, Middle Aged, Polymorphism, Single Nucleotide, Risk Factors, Genetic Predisposition to Disease, Multiple Myeloma genetics, Myeloproliferative Disorders genetics
- Abstract
Myeloproliferative neoplasms (MPNs) are a group of diseases that cause myeloid hematopoietic cells to overproliferate. Epidemiological and familial studies suggest that genetic factors contribute to the risk of developing MPN, but the genetic susceptibility of MPN is still not well known. Indeed, only few loci are known to have a clear role in the predisposition to this disease. Some studies reported a diagnosis of MPNs and multiple myeloma (MM) in the same patients, but the biological causes are still unclear. We tested the hypothesis that the two diseases share at least partly the same genetic risk loci. In the context of a European multicenter study with 460 cases and 880 controls, we analyzed the effect of the known MM risk loci, individually and in a polygenic risk score (PRS). The most significant result was obtained among patients with chronic myeloid leukemia (CML) for PS0RS1C1-rs2285803, which showed to be associated with an increased risk (OR = 3.28, 95% CI 1.79-6.02, P = .00012, P = .00276 when taking into account multiple testing). Additionally, the PRS showed an association with MPN risk when comparing the last with the first quartile of the PRS (OR = 2.39, 95% CI 1.64-3.48, P = 5.98 × 10
-6 ). In conclusion, our results suggest a potential common genetic background between MPN and MM, which needs to be further investigated., (© 2020 UICC.)- Published
- 2021
- Full Text
- View/download PDF
7. Genetic polymorphisms associated with telomere length and risk of developing myeloproliferative neoplasms.
- Author
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Giaccherini M, Macauda A, Sgherza N, Sainz J, Gemignani F, Maldonado JMS, Jurado M, Tavano F, Mazur G, Jerez A, Góra-Tybor J, Gołos A, Mohedo FH, Lopez JM, Várkonyi J, Spadano R, Butrym A, Canzian F, and Campa D
- Subjects
- Aged, Female, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Myeloproliferative Disorders etiology, Risk Factors, Myeloproliferative Disorders genetics, Polymorphism, Single Nucleotide, Telomere Homeostasis
- Abstract
Telomere length measured in leukocyte (LTL) has been found to be associated with the risk of developing several cancer types, including myeloproliferative neoplasms (MPNs). LTL is genetically determined by, at least, 11 SNPs previously shown to influence LTL. Their combination in a score has been used as a genetic instrument to measure LTL and evaluate the causative association between LTL and the risk of several cancer types. We tested, for the first time, the "teloscore" in 480 MPN patients and 909 healthy controls in a European multi-center case-control study. We found an increased risk to develop MPNs with longer genetically determined telomeres (OR = 1.82, 95% CI 1.24-2.68, P = 2.21 × 10
-3 , comparing the highest with the lowest quintile of the teloscore distribution). Analyzing the SNPs individually we confirm the association between TERT-rs2736100-C allele and increased risk of developing MPNs and we report a novel association of the OBFC1-rs9420907-C variant with higher MPN risk (ORallelic = 1.43; 95% CI 1.15-1.77; P = 1.35 × 10-3 ). Consistently with the results obtained with the teloscore, both risk alleles are also associated with longer LTL. In conclusion, our results suggest that genetically determined longer telomeres could be a risk marker for MPN development.- Published
- 2020
- Full Text
- View/download PDF
8. Managing chronic myeloid leukemia for treatment-free remission: a proposal from the GIMEMA CML WP.
- Author
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Baccarani M, Abruzzese E, Accurso V, Albano F, Annunziata M, Barulli S, Beltrami G, Bergamaschi M, Binotto G, Bocchia M, Caocci G, Capodanno I, Cavazzini F, Cedrone M, Cerrano M, Crugnola M, D'Adda M, Elena C, Fava C, Fazi P, Fozza C, Galimberti S, Giai V, Gozzini A, Gugliotta G, Iurlo A, La Barba G, Levato L, Lucchesi A, Luciano L, Lunghi F, Lunghi M, Malagola M, Marasca R, Martino B, Melpignano A, Miggiano MC, Montefusco E, Musolino C, Palmieri F, Pregno P, Rapezzi D, Rege-Cambrin G, Rupoli S, Salvucci M, Sancetta R, Sica S, Spadano R, Stagno F, Tiribelli M, Tomassetti S, Trabacchi E, Bonifacio M, Breccia M, Castagnetti F, Pane F, Russo D, Saglio G, Soverini S, Vigneri P, and Rosti G
- Subjects
- Adolescent, Adult, Antineoplastic Combined Chemotherapy Protocols adverse effects, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Disease Management, Female, Fusion Proteins, bcr-abl genetics, Health Care Costs, Health Care Surveys, Humans, Italy epidemiology, Leukemia, Myelogenous, Chronic, BCR-ABL Positive diagnosis, Leukemia, Myelogenous, Chronic, BCR-ABL Positive etiology, Male, Middle Aged, Pregnancy, Protein Kinase Inhibitors administration & dosage, Protein Kinase Inhibitors adverse effects, Protein Kinase Inhibitors therapeutic use, Remission Induction, Retreatment, Treatment Outcome, Young Adult, Leukemia, Myelogenous, Chronic, BCR-ABL Positive epidemiology, Leukemia, Myelogenous, Chronic, BCR-ABL Positive therapy
- Abstract
Several papers authored by international experts have proposed recommendations on the management of BCR-ABL1+ chronic myeloid leukemia (CML). Following these recommendations, survival of CML patients has become very close to normal. The next, ambitious, step is to bring as many patients as possible into a condition of treatment-free remission (TFR). The Gruppo Italiano Malattie EMatologiche dell'Adulto (GIMEMA; Italian Group for Hematologic Diseases of the Adult) CML Working Party (WP) has developed a project aimed at selecting the treatment policies that may increase the probability of TFR, taking into account 4 variables: the need for TFR, the tyrosine kinase inhibitors (TKIs), the characteristics of leukemia, and the patient. A Delphi-like method was used to reach a consensus among the representatives of 50 centers of the CML WP. A consensus was reached on the assessment of disease risk (EUTOS Long Term Survival [ELTS] score), on the definition of the most appropriate age boundaries for the choice of first-line treatment, on the choice of the TKI for first-line treatment, and on the definition of the responses that do not require a change of the TKI (BCR-ABL1 ≤10% at 3 months, ≤1% at 6 months, ≤0.1% at 12 months, ≤0.01% at 24 months), and of the responses that require a change of the TKI, when the goal is TFR (BCR-ABL1 >10% at 3 and 6 months, >1% at 12 months, and >0.1% at 24 months). These suggestions may help optimize the treatment strategy for TFR., (© 2019 by The American Society of Hematology.)
- Published
- 2019
- Full Text
- View/download PDF
9. Hairy cell leukaemia and venous thromboembolism: a case report and review of the literature.
- Author
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Vazzana N, Spadano R, Sestili S, Toto V, Falorio S, Catinella V, Angrilli F, and Dragani A
- Subjects
- Humans, Male, Middle Aged, Leukemia, Hairy Cell blood, Leukemia, Hairy Cell complications, Leukemia, Hairy Cell therapy, Venous Thromboembolism blood, Venous Thromboembolism complications, Venous Thromboembolism therapy
- Published
- 2014
- Full Text
- View/download PDF
10. TET2 mutations in Ph-negative myeloproliferative neoplasms: identification of three novel mutations and relationship with clinical and laboratory findings.
- Author
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Patriarca A, Colaizzo D, Tiscia G, Spadano R, Di Zacomo S, Spadano A, Villanova I, Margaglione M, Grandone E, and Dragani A
- Subjects
- Adult, Aged, Aged, 80 and over, Cohort Studies, DNA Mutational Analysis, Dioxygenases, Female, Humans, Male, Middle Aged, Myeloproliferative Disorders complications, Thrombosis complications, Thrombosis genetics, DNA-Binding Proteins genetics, Mutation genetics, Myeloproliferative Disorders diagnosis, Myeloproliferative Disorders genetics, Philadelphia Chromosome, Proto-Oncogene Proteins genetics
- Abstract
High-throughput DNA sequence analysis was used to screen for TET2 mutations in peripheral blood derived DNA from 97 patients with BCR-ABL-negative myeloproliferative neoplasms (MPNs). Overall six mutations in the coding region of the gene were identified in 7 patients with an overall mutational frequency of 7.2%. In polycythemia vera patients (n = 25) 2 mutations were identified (8%), and in those with essential thrombocythemia (n = 55) 2 mutations (3.6%); in those with unclassifiable MPN (n = 8) 3 mutations (37.5%). No primary myelofibrosis patients (n = 6) harboured TET2 mutations. Three unreported mutations were identified (p.P177fs, p.C1298del, and p.P411del), the first two in patients with unclassifiable MPN, the last in a patient with essential thrombocythemia. On multivariate analysis the diagnosis of an unclassifiable MPN was significantly related to the presence of TET2 mutations (P = 0.02; OR: 2.81; 95% CI 1.11-7.06). We conclude that TET2 mutations occur in both JAK2 V617F-positive and -negative MPNs and are more frequent in MPN-U patients. This could represent the biological link between the different classes of myeloid malignancies.
- Published
- 2013
- Full Text
- View/download PDF
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