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Littérature scientifique sur le sujet « Ph-negative chronic myeloproliferative neoplasms »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Ph-negative chronic myeloproliferative neoplasms"

Мурзабекова, М. А., Я. М. Марченко, Д. И. Шихбабаева, and О. Ю. Виноградова. "Genetic Aspects Classical Ph-negative Myeloproliferative Neoplasms (Literature Review)." Гематология. Трансфузиология. Восточная Европа 10, no. 2 (2024): 210–18. http://dx.doi.org/10.34883/pi.2024.10.2.001.

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Рh-негативные миелопролиферативные новообразования – это группа заболеваний, которые характеризуются клональной пролиферацией одной или нескольких клеточных линий миелоидных предшественников, а также соединительнотканных компонентов костного мозга и сопровождаются изменениями показателей крови. В соответствии с классификацией Всемирной организации здравоохранения 2022 года к Ph-негативным новообразованиям относятся истинная полицитемия, эссенциальная тромбоцитемия, первичный миелофиброз, хронический нейтрофильный лейкоз, хронический эозинофильный лейкоз, ювенильный миеломоноцитарный лейкоз и м

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Martinkov, V. N., D. K. Novik, I. V. Veyalkin, A. E. Silin, and I. A. Iskrov. "The incidence of Ph-negative chronic myeloproliferative neoplasms in Belarus." Russian journal of hematology and transfusiology 68, no. 3 (2023): 363–72. http://dx.doi.org/10.35754/0234-5730-2023-68-3-363-372.

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Introduction. Ph-negative myeloproliferative neoplasms (MPN) are chronic clonal disorders characterized by the proliferation of mature cells from one or more myeloid cell lines. These disorders include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The incidence of classical Ph-negative MPN varies significantly throughout the world. These differences may be due to geographical or population features, as well as due to differences in methods of diagnosis and recording. Aim: to determine incidence of Ph-negative MPN in Belarus. Materials and methods. Dat

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Polyakov, A. S., V. V. Tyrenko, Ya A. Noskov, D. K. Zhogolev, and A. V. Kovalev. "Clinical and laboratory features of different types of interferon therapy classic Ph-negative myeloproliferative neoplasms." Genes & Cells 11, no. 3 (2016): 153–61. http://dx.doi.org/10.23868/gc120618.

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Chronic myeloproliferative neoplasms are a group of disorders characterized by clonal disturbance of pluripotent bone marrow stem cells, leading to an excessive increase in hematopoietic cells that retain the ability to differentiate. Modern screening techniques have made changes to the current view of the epidemiology of myeloproliferative neoplasms. Recently, more and more researches are found with the median age below 50 years, and sometimes less than 40 years. This circumstance determines the need to improve therapy with the use of interferon-а. A new stage in the treatment of myeloprolife

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Bittencourt, Rosane Isabel, Jose Vassallo, Maria de Lourdes Lopes Ferrari Chauffaille, et al. "Philadelphia-negative chronic myeloproliferative neoplasms." Revista Brasileira de Hematologia e Hemoterapia 34, no. 2 (2012): 140–49. http://dx.doi.org/10.5581/1516-8484.20120034.

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Tarakanova, A. V., D. S. Abramov, A. V. Pshonkin, and D. M. Konovalov. "Pathomorphological diagnosis of Ph-negative chronic myeloproliferative neoplasms in children." Pediatric Hematology/Oncology and Immunopathology 23, no. 3 (2024): 123–29. http://dx.doi.org/10.24287/1726-1708-2024-23-3-123-129.

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BCR::ABL/Ph-negative chronic myeloproliferative neoplasms (CMPN) in children differ from those in adults in clinical manifestations and genetic alterations. Taking into account the well-known physiology of hematopoiesis in children, it seems important to compare the histological features of CMPN in pediatric patients with the criteria for the diagnosis of these diseases in adults specified in the World Health Organization (WHO) classification. In pediatric practice, the interpretation of changes in hematopoiesis in patients with CMPN without any established driver mutation has a particular imp

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Ryabukhina, Yu E., P. A. Zeynalova, O. I. Timofeeva, et al. "Combination approach to diagnosis and treatment of an elderly patient with chronic Ph-negative myeloproliferative neoplasm and concomitant surgical pathology. Clinical observation." MD-Onco 1, no. 1 (2021): 61–65. http://dx.doi.org/10.17650/2782-3202-2021-1-1-61-65.

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Chronic myeloproliferative neoplasms (CMPN), Ph-negative, are of clonal nature, develop on the level of hematopoietic stem cell and are characterized by proliferation of one or more hematopoietic pathways. Currently, the group of Ph-negative CMPN includes essential thrombocythemia, primary myelofibrosis, polycythemia vera, myeloproliferative neoplasm unclassifiable.Identification of mutations in the Jak2 (V617F), CALR, and MPL genes extended understanding of biological features of Ph-negative CMPN and improved differential diagnosis of myeloid neoplasms. Nonetheless, clinical practice still en

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Hasserjian, Robert P. "The spectrum of Ph-negative disease: CNL and CSF3R-related disorders." Hematology 2024, no. 1 (2024): 270–78. https://doi.org/10.1182/hematology.2024000555.

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Abstract Chronic neutrophilic leukemia (CNL) is a very rare myeloid neoplasm characterized by peripheral blood neutrophilia and a hypercellular marrow with increased granulopoiesis. An activating mutation in CSF3R is present in 80% to 90% of cases. CNL displays some biological overlap in terms of clinical presentation and behavior, as well as genetic profile, with several other myeloid neoplasms, particularly myelodysplastic/myeloproliferative neoplasms (MDS/MPN) and other MPN. Distinguishing these related entities can be challenging, requires close attention to peripheral blood and bone marro

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Nann, Dominik, and Falko Fend. "Synoptic Diagnostics of Myeloproliferative Neoplasms: Morphology and Molecular Genetics." Cancers 13, no. 14 (2021): 3528. http://dx.doi.org/10.3390/cancers13143528.

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The diagnosis of a myeloid neoplasm relies on a combination of clinical, morphological, immunophenotypic and genetic features, and an integrated, multimodality approach is needed for precise classification. The basic diagnostics of myeloid neoplasms still rely on cell counts and morphology of peripheral blood and bone marrow aspirate, flow cytometry, cytogenetics and bone marrow trephine biopsy, but particularly in the setting of Ph− myeloproliferative neoplasms (MPN), the trephine biopsy has a crucial role. Nowadays, molecular studies are of great importance in confirming or refining a diagno

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Polushkina, Lyubov, Irina Martynkevich, Vasily Shuvaev, et al. "Genetic and Epigenetic Alterations of Ph-Negative Myeloproliferative Neoplasms." Blood 124, no. 21 (2014): 5549. http://dx.doi.org/10.1182/blood.v124.21.5549.5549.

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Abstract Objectives and background: Genetic mutations result in abnormalities of myelopoietic proteins and lie in the basis of Ph-negative myeloproliferative neoplasms (MPNs) development and its subsequent progression. Several somatic mutations in JAK2, MPL, TET2, EZH2, ASXL1, CBL, IDH1, IDH2, IKZF1 genes were detected in chronic and blastic phase MPNs. Recent studies have revealed a number of epigenetic alterations that contribute to Ph-negative MPNs pathogenesis and determine the clinical outcome. Mutations involving the EZH2 gene are thought to result in loss of methyltransferase activity s

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Paciaroni, Katia, Selenia Campagna, Nicoletta Villiva', et al. "CO-OCCURRENCE OF JAK2/CALR-POSITIVE MYELOPROLIFERATIVE DISORDER AND BCR-ABL-POSITIVE CHRONIC MYELOGENOUS LEUKAEMIA TREATED WITH COMBINATION OF TYROSINE KINASE INHIBITORS AND RUXOLITINIB." Mediterranean Journal of Hematology and Infectious Diseases 17, no. 1 (2025): e2025023. https://doi.org/10.4084/mjhid.2025.023.

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The concomitant presence of BCR-Abl1 and JAK2/CALR mutations in Myeloproliferative neoplasms (MPNs) is rare. The clinical presentation of Chronic Myelogenous Leukemia (CML) and Ph-negative MPN may vary, but CML seems to play a dominant role, so patients usually receive treatment with tyrosine kinase inhibitor (TKI) only. The second Ph-negative MPN becomes evident under the selective pressure of the TK.I.

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Thèses sur le sujet "Ph-negative chronic myeloproliferative neoplasms"

MINNUCCI, GIULIA. "Development and clinical validation of a novel and NON-PCR based method for the detection of the JAK2V617F mutation in chronic mycloproliferative neoplasms." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29394.

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Myeloproliferative Neoplasms (MPNs) are haematologic disorders of myeloid progenitor cells characterized by the frequent presence of an acquired activating mutation in exon 14 of the Janus kinase 2, consisting in a Valine to Phenilalanine substitution at codon 617 (JAK2V617F). The kinase activity of mutated JAK2 is constitutively activated, inducing uncontrolled cell proliferation and resistance to apoptosis. JAK2V617F is found in 95% of Polycythemia Vera (PV), 50% of Idiopathic Myelofibrosis (IMF), and 20-40% of Essential Thrombocythemia (ET), the three diseases belonging to MPNs, as describe

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Perricone, Margherita <1987&gt. "Characterization of Philadelphia-negative Chronic Myeloproliferative Neoplasms: identification of novel biomarkers by Next Generation Sequencing and study of interactions between hematopoietic stem cell and the inflammatory cell micro-environment." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amsdottorato.unibo.it/8358/1/PhD%20Thesis_MPerricone_final.pdf.

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Myeloproliferative Neoplasms (MPN) are a heterogeneous group of hematological malignancies, consisting in clonal disorders of the hematopoietic stem/progenitor cell (HSC/PC). Molecular alterations and inflammatory microenvironment represent the two main etiopathogenic factors of MPN. The aim of this study was the molecular characterization of MPN patients and the study of interactions between HSC/PC and the inflammatory cell micro-environment. We investigated young (<40 years at diagnosis) ET and early-PMF patients, and patients with a JAK2V617F allele burden (AB) <3%, demonstrating that i

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Orvain, Corentin. "Elaboration de nouveaux outils pour le diagnostic et le pronostic des patients atteints de syndrome myéloprolifératif. Circulating Cd34+ cell count differentiates primary myelofibrosis from other Philadelphia-negative myeloproliferative neoplasms: a pragmatic study Sequential mutational evaluation of CALR-mutated myelopro-liferative neoplasms with thrombocytosis reveals an associa-tion between CALR allele burden evolution and diseaseprogression." Thesis, Angers, 2019. http://www.theses.fr/2019ANGE0043.

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Plusieurs scores pronostiques ont été élaboré chez les patients atteints de leucémie myéloïde chronique (LMC) sans qu’un lien n’ait été établi entre ces scores et la biologie de la LMC. Nous montrons que les patients de mauvais pronostic ont une expression accrue de GATA2, en corrélation avec les taux de basophiles et de plaquettes au diagnostic, paramètres utilisés dans le calcul des scores pronostiques, et à l’expression de gènes impliqués dans le fonctionnement des basophiles. Cette expression augmente lors de la transformation sur un versant myéloïde. Alors qu’un certain nombre de patients

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PIERI, LISA. "Study of new molecular alterations on Philadelphia-negative chronic myeloproliferative neoplasms." Doctoral thesis, 2013. http://hdl.handle.net/2158/804681.

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Lo studio si è basato su tecnologia di SNP array per identificare regioni cromosomiche oggetto di alterazioni di copy number in un’ampia casisitica di pazienti con neoplasie mieloproliferative croniche Ph-negative, sia nella fase cronica di malattia sia soprattutto nella transizione ad una leucemia acuta. Sulla base di una di queste anomalie identificate, sono poi state condotte ulteriori ricerche che hanno permesso di identificare una nuova anomalia molecolare, non descritta in precedenza, che genera un trascritto chimerico di fusione che è in avanzata fase di caratterizzazione. In this stud

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Livres sur le sujet "Ph-negative chronic myeloproliferative neoplasms"

Steensma, David P. Malignant Hematology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0296.

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The hematologic neoplasms include lymphoproliferative disorders (eg, chronic lymphocytic leukemia [CLL]/small lymphocytic lymphoma [SLL], large granular lymphocyte leukemia, hairy cell leukemia [HCL], Hodgkin lymphoma, non-Hodgkin lymphoma), plasma cell disorders (multiple myeloma, light chain amyloidosis, Waldenström macroglobulinemia, POEMS syndrome, heavy chain disease, plasmacytoma), chronic myeloid neoplasms (chronic myeloid leukemia, the BCR/ABL-negative myeloproliferative neoplasms, myelodysplastic syndromes), and acute leukemia (acute myeloid leukemia, acute lymphocytic leukemia). In a

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Chapitres de livres sur le sujet "Ph-negative chronic myeloproliferative neoplasms"

Marchetti, Monia. "Ph-Negative Chronic Myeloproliferative Neoplasms." In Reference Module in Biomedical Sciences. Elsevier, 2024. http://dx.doi.org/10.1016/b978-0-443-15717-2.00015-9.

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Tantravahi, Srinivas K., Jamshid S. Khorashad, and Michael W. Deininger. "Genomic landscape of myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0002.

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The discovery of the Philadelphia chromosome (Ph) and BCR-ABL1 fusion gene in chronic myeloid leukaemia (CML) was a first step in understanding the genetic basis of myeloproliferative neoplasms (MPN), but it took more than 20 years until the molecular basis of Ph<sup>–</sup> MPN was unravelled with the identification of mutually exclusive mutations in JAK2, MPL, and CALR. The common effect of these mutations, activation of JAK/STAT signalling, informed the therapeutic development of JAK kinase inhibitors. Additional mutations in epigenetic modifier, mRNA splicing, and transcriptional regulator

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Fleischman, Angela G., and Richard A. Van Etten. "Pathogenesis of myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0003.

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The myeloproliferative neoplasms (MPN) were first grouped together by Dameshek in 1951 based upon their similar clinical characteristics. Since that time, and particularly over the past decade, molecular biological and genetic investigation into the pathogenesis of MPN has revealed their shared stem cell nature, a common pathophysiological theme of aberrant cytokine signalling through dysregulated tyrosine kinases that drives the overproduction of maturing myeloid cells, and, as in other myeloid neoplasms, a major modifying role for loss of function mutations in epigenetic regulatory proteins.

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Rambaldi, Alessandro, and Nicholas Kröger. "Stem cell transplantation for BCR-ABL1-positive and negative myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0016.

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The indication to allogeneic stem cell transplantation has changed in the treatment strategy of chronic myeloid leukaemia (CML) and myelofibrosis (MF). The introduction of tyrosine kinase inhibitors has confined the indication to transplant only to the very few CML patients who fail the medical treatment or progress to a blastic phase of the disease. Nonetheless, a distinct group of CML patients still require allogeneic transplant that remains a curable treatment options even for these otherwise incurable patients. On the other hand, the allogeneic transplant activity for myelofibrosis is grow

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Najfeld, Vesna. "Conventional and Molecular Cytogenetics of Ph-Negative Chronic Myeloproliferative Disorders." In Myeloproliferative Disorders. CRC Press, 2007. http://dx.doi.org/10.3109/9781420061635-3.

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Aruch, Daniel, and Ronald Hoffman. "Thrombocytosis and essential thrombocythaemia." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0518.

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The term thrombocytosis refers to a platelet count elevated above 450 × 10<sup>9</sup>/litre, which can be (1) primary—including essential thrombocythaemia, chronic myeloid leukaemia, polycythaemia vera, and myelodysplastic syndromes; or (2) secondary—including iron deficiency, infection, blood loss, and malignancy. Essential thrombocythaemia: aetiology—the JAK2 V617F missense mutation typical of polycythaemia vera is found in about 50% of cases. In addition, 10% of patients have a mutation in the thrombopoietin receptor gene, MPL, and 30% have a mutation in calreticulin (CALR). Approximately

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Musteata, Vasile, and Valentina Stratan. "Diagnosis and Management of Chronic BCR-ABL-Positive and BCR-ABL-Negative Myeloproliferative Neoplasms in Elderly Patients: An Approach towards Hematologic Oncology and Public Health." In Issues and Developments in Medicine and Medical Research Vol. 5. Book Publisher International (a part of SCIENCEDOMAIN International), 2022. http://dx.doi.org/10.9734/bpi/idmmr/v5/2405c.

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Actes de conférences sur le sujet "Ph-negative chronic myeloproliferative neoplasms"

Oh, Stephen T., Jacob M. Zahn, Erin F. Simonds, et al. "Abstract B6: Identification of novel mutations in the inhibitory adaptor protein LNK in patients with JAK2 V617F-negative and -positive chronic myeloproliferative neoplasms." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-b6.

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