Relevant bibliographies by topics / MiRna, Primary Myelofibrosis, Myeloproliferative Neoplasms

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Academic literature on the topic 'MiRna, Primary Myelofibrosis, Myeloproliferative Neoplasms'

Author: Grafiati
Published: 10 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "MiRna, Primary Myelofibrosis, Myeloproliferative Neoplasms"

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Khaleel, Sarah I., and Jaffar N. AlAlsaidissa. "Analysis of MicroRNA -155-5p Expression in Patients with Primary Myelofibrosis." Journal of the Faculty of Medicine Baghdad 66, no. 4 (2024): 487–92. https://doi.org/10.32007/jfacmedbaghdad.6642400.

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Background: Primary myelofibrosis is a chronic myeloproliferative neoplasm characterized by abnormal megakaryocyte proliferation and fibrosis that destroys healthy bone marrow. This results in extramedullary hematopoiesis, variable blood cell deficiencies, hepatosplenomegaly, general symptoms, progression to leukemia, and a reduced lifespan. Myelofibrosis can occur as a de novo myeloproliferative neoplastic disorder or evolve from other myeloproliferative neoplasms, including Polycythemia Vera or Essential Thrombocytosis. MicroRNAs (miRNAs) are short, non-protein-coding RNA molecules, typicall
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Manaila, Roxana, Vlad Moisoiu, Erik Knutsen, Mihnea P. Dragomir, and George A. Calin. "Diagnostic and Therapeutic MicroRNAs in Primary Myelofibrosis." Proceedings of the Singapore National Academy of Science 14, no. 02 (2020): 91–109. http://dx.doi.org/10.1142/s2591722620400074.

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Primary myelofibrosis (PMF) is a pluripotent hematopoietic stem cell-derived malignancy, included in the heterogeneous group of myeloproliferative neoplasms (MPNs). PMF diagnosis is based on a composite assessment of clinical and laboratory data. The three major diagnostic criteria are: screening for driver mutations, exclusion of other conditions that can cause myelofibrosis, and bone marrow biopsy displaying megakaryocyte changes and fibrosis. PMF treatment options are only partially disease-modifying and consist mainly of symptom control. Recently, a new targeted therapy was introduced for
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Norfo, Ruggiero, Roberta Zini, Valentina Pennucci, et al. "Regulatory Mrna/Microrna Networks in CD34+ Cells From Primary Myelofibrosis." Blood 120, no. 21 (2012): 2854. http://dx.doi.org/10.1182/blood.v120.21.2854.2854.

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Abstract Abstract 2854 Molecular mechanisms underlying Philadephia-negative myeloproliferative neoplasm (MPN) pathogenesis were partially unraveled in 2005–2006 with the identification of somatic gain-of-function of JAK2 and MPL, after which many other mutated genes were found. Recently, several new molecular pathogenetic mechanisms were identified. Among them, aberrant microRNA (miRNA) expression especially seems to add to the molecular complexity of MPNs, as specific miRNA signatures capable of discriminating MPN cells from those of normal donors were previously reported (P. Guglielmelli et
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Zini, Roberta, Ruggiero Norfo, Valentina Pennucci, et al. "Integrative Analysis Of mRNA/miRNA Expression Profiles Identified JARID2 As a Shared Target Of Deregulated Mirnas In Primary Myelofibrosis." Blood 122, no. 21 (2013): 1600. http://dx.doi.org/10.1182/blood.v122.21.1600.1600.

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Abstract Ph-negative myeloproliferative neoplasms (MPNs) are characterized by many somatic mutations which have already been shown useful in the prognostic assessment of MPN patients [A.M. Vannucchi et al., Leukemia, 2013]. Moreover, aberrant microRNA (miRNA) expression seems to add to the molecular complexity of MPNs, as specific miRNA signatures capable of discriminating MPN cells from those of normal donors were previously reported [P. Guglielmelli et al., Exp Hematol, 2007]. In order to have a comprehensive picture of miRNA deregulation and its relationship with differential gene expressio
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Harada, Kayo Shirado, Kazuhiko Ikeda, Kazuei Ogawa, et al. "The Role Of Deregulated HMGA2 Expression With Promoter Methylation Of p16 In Myeloproliferative Neoplasms." Blood 122, no. 21 (2013): 1606. http://dx.doi.org/10.1182/blood.v122.21.1606.1606.

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Abstract Myeloproliferative Neoplasms (MPNs) are characterized by clonal proliferative hematopoiesis with increased mature blood cells. The signal-activating mutations such as JAK2V617F increase blood cells, but it remains uncertain how an abnormal hematopoietic cell clone expands in MPNs. We have recently showed that overexpression of the high mobility group AT-hook 2 (HMGA2) causes proliferative hematopoiesis with providing a clonal growth advantage to hematopoietic cells in mice (Ikeda et al, Blood, 2011), suggesting the possibility that HMGA2 contributes to the pathogenesis of MPNs. Howeve
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Rontauroli, Sebastiano, Ruggiero Norfo, Valentina Pennucci, et al. "MiR-494-3p Overexpression Leads to SOCS6 Downregulation and Supports Megakaryocytopoiesis in Primary Myelofibrosis CD34+ Hematopoietic Stem/Progenitor Cells." Blood 128, no. 22 (2016): 4272. http://dx.doi.org/10.1182/blood.v128.22.4272.4272.

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Abstract Primary Myelofibrosis (PMF) belongs to the Philadelphia negative Myeloproliferative Neoplasms (MPNs) and is characterized by hematopoietic stem-cell derived clonal myeloproliferation, involving especially megakaryocyte (MK) lineage, bone marrow fibrosis and extramedullary hematopoiesis. Recent studies have suggested that alterations in miRNAs expression could play a critical role in MPN's pathogenesis. In order to shed some light on this issue, we have previously performed the integrative analysis (IA) of gene and miRNA expression profiles of PMF CD34+ hematopoietic stem/progenitor ce
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Harada, Kayo Shirado, Kazuhiko Ikeda, Kazuei Ogawa, Hiroshi Ohkawara, and Yasuchika Takeishi. "Dysregulation of the Let-7/HMGA2 Axis with Methylation of p16 Promoter As a Possible Target of Histone Deacetylase Inhibitor in Myeloproliferative Neoplasms." Blood 124, no. 21 (2014): 3213. http://dx.doi.org/10.1182/blood.v124.21.3213.3213.

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Abstract Myeloproliferative neoplasms (MPNs), including polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF), are clonal hematological disorders characterized by proliferation of mature blood cells. Recently, several agents that influence epigenetic modifications, such as histone deacetylase inhibitors (HDACi), as well as JAK2 inhibitors, have been investigated for high-risk MPNs. For example, an HDACi, panobinostat has shown significant efficacy including nearly complete response in PMF (Mascarenhas et al, BJH, 2013), but molecular targets of HDACi remain lar
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Visani, Giuseppe, Alessandro Isidori, Maria Rosaria Sapienza, et al. "Identification of Novel Cryptic Chromosomal Abnormalities in Primary Myelofibrosis by Single-Nucleotide Polymorphism Oligonucleotide Microarray." Blood 114, no. 22 (2009): 1890. http://dx.doi.org/10.1182/blood.v114.22.1890.1890.

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Abstract Abstract 1890 Poster Board I-913 Background. Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm (MPN) characterised by a proliferation of predominantly megakaryocytes and granulocytes in bone marrow that in fully developed disease is replaced by fibrous tissue. At molecular level, no specific defect has been identified yet. Cytogenetic abnormalities occur in up to 30% of patients, the commonest including del(13)(q12-22), der(6)t(1;6)(q21-23;p21.3), del (20q), and partial trisomy 1q. In addition, approximately 50% of patients with PMF exhibit a single, recurrent, somat
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Costa Villela, Neysimelia, Gustavo Zamperlini, Patrícia Shimoda Ikeuti, Roseane Vasconcelos Gouveia, Simone De Castro Resende Franco, and Luiz Fernando Lopes. "Myeloproliferative neoplasms." JOURNAL OF BONE MARROW TRANSPLANTATION AND CELLULAR THERAPY 2, no. 4 (2021): 129. http://dx.doi.org/10.46765/2675-374x.2021v2n4p129.

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 In addition to the chronic myeloid leukemia (CML) BCR-ABL1+, classic myeloproliferative neoplasms include polycythemia vera, essential thrombocythemia and primary myelofibrosis. These have a very low incidence in the pediatric age group and there is no consensus on treatment in children.
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Stein, Brady L., and Alison R. Moliterno. "Primary Myelofibrosis and the Myeloproliferative Neoplasms." JAMA 303, no. 24 (2010): 2513. http://dx.doi.org/10.1001/jama.2010.853.

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Dissertations / Theses on the topic "MiRna, Primary Myelofibrosis, Myeloproliferative Neoplasms"

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Pedrazzani, Fabiane Spagnol. "Impacto da análise molecular da mutação JAK2V617F no diagnóstico de neoplasias mieloproliferativas crônicas de acordo com os critérios da OMS 2016." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/157653.

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As neoplasias mieloproliferativas (NMPs) são um grupo de doenças derivadas de uma transformação clonal de célula tronco hematopoiéticas no qual a linhagem celular mielóide é predominantemente expandida no sangue periférico. As NMPs Philadelphia-negativas incluem policitemia vera (PV), trombocitemia essencial (TE) e mielofibrose primária (MFP) que compartilham muitas características hematológicas, clínicas e evolutivas. A mutação da JAK2 (JAK2V617F) está presente em cerca de 95% dos pacientes com PV, entre 50 a 70% com TE e 40 a 50% com MFP. No entanto, os testes moleculares para diagnóstico sã
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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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MANNARELLI, CARMELA. "“MiRNA expression in Primary Myelofibrosis: characterization and pathophysiology implications”." Doctoral thesis, 2016. http://hdl.handle.net/2158/1039412.

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Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by megakaryocyte (MK) hyperplasia, bone marrow fibrosis, and abnormal stem cell trafficking. PMF may be associated with somatic mutations, about 90% of patients harbor one of three “driver” mutations, with mutational frequencies of approximately 60%, 22% and 6% for JAK2, CALR and MPL, respectively. Other “non-driver” mutations have also been described in PMF involving different cellular targets such as epigenetic regulatory pathways genes (ASXL1, DNMT3A, EZH2, IDH1 and IDH2, TET2), splicing factor genes (SRSF2, SF3B1) a
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Books on the topic "MiRna, Primary Myelofibrosis, Myeloproliferative Neoplasms"

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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Myeloproliferative neoplasms. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0007.

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Myeloproliferative neoplasms (MPNs) - Pathogenesis of the MPNs - Polycythaemia vera (PV) - Natural history of PV - Management of PV - Secondary erythrocytosis - Relative erythrocytosis - Idiopathic erythrocytosis - Essential thrombocythaemia - Reactive thrombocytosis - Primary myelofibrosis - Chronic neutrophilic leukaemia - Eosinophilic syndromes and neoplasms - Mastocytosis (mast cell disease) - Systemic mastocytosis - MPN—unclassifiable
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Mammit Kaur. Myeloproliferative neoplasms. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0007_update_001.

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Myeloproliferative neoplasms (MPNs) - Pathogenesis of the MPNs - Polycythaemia vera (PV) - Natural history of PV - Management of PV - Secondary erythrocytosis - Relative erythrocytosis - Idiopathic erythrocytosis - Essential thrombocythaemia - Reactive thrombocytosis - Primary myelofibrosis - Chronic neutrophilic leukaemia - Eosinophilic syndromes and neoplasms - Mastocytosis (mast cell disease) - Systemic mastocytosis - MPN—unclassifiable
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Mughal, Tariq I., and Tiziano Barbui, eds. Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.001.0001.

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Our understanding of myeloproliferative neoplasms (MPN) disorders, a group of clonal haematological malignancies characterized by excessive accumulation of one or more myeloid cell lineages, has grown considerably over the past four decades. Even more importantly is the speed at which many of these findings were translated to accord survival benefits to our patients with MPN, in particular chronic myeloid leukaemia (CML), polycythaemia vera (PV), essential thrombocythaemia (ET), and primary myelofibrosis (PMF). This text offers a detailed evidence-based guide to MPN in an easily accessible for
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Collins, Graham, and Chris Bunch. Myeloproliferative disorders. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0291.

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Myeloproliferative disorders (also called myeloproliferative neoplasms) can be defined as clonal haematopoietic disorders resulting in excess production of one or more blood cell lineage. The four main conditions are primary polycythaemia, which is characterized by excess red-cell production; essential thrombocythaemia, which is characterized by excess platelet production; chronic myeloid leukaemia, which is characterized by excess granulocyte production; and myelofibrosis, which is characterized by excess megakaryocyte proliferation, which results in a reactive fibroblast proliferation causin
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Book chapters on the topic "MiRna, Primary Myelofibrosis, Myeloproliferative Neoplasms"

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Barosi, Giovanni. "Conventional and Investigational Therapy for Primary Myelofibrosis." In Myeloproliferative Neoplasms. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_6.

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Tefferi, Ayalew. "Myeloproliferative Neoplasms: Essential Thrombocythemia, Polycythemia Vera, and Primary Myelofibrosis." In Practical Hemostasis and Thrombosis. Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444306286.ch14.

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Tibes, Raoul, Gurcharan Singh Khera, and Ruben A. Mesa. "Myeloproliferative Neoplasms: Chronic Myelogenous Leukemia, Polycythemia Vera, Essential Thrombocythemia, and Primary Myelofibrosis." In Textbook of Uncommon Cancer. John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118464557.ch47.

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Harrison, Claire, Yan Beauverd, and Donal McLorran. "Myelofibrosis." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0009.

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The World Health Organization (WHO) classification defines myelofibrosis (MF) to comprise of the three principal subtypes, primary myelofibrosis, post-polycythaemia vera myelofibrosis, and post-essential thrombocythaemia. Each subtype appears to exhibit a similar pathogenesis, clinical presentation, evolution, and treatment. The critical driver mutations involved in the pathogenesis are be JAK2, MPL, or CALR; mutations in the splicing machinery genes, the epigenome, transcription factors, and dysregulation in the haematopoietic stem cell niche also play pathogenetic roles. Myelofibrosis is a p
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Abdelwahab, Omar, Raajit Rampal, Catriona Jamieson, and Tariq I. Mughal. "Transformation of myeloproliferative neoplasms to acute leukaemia." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0014.

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Clinically chronic myeloproliferative neoplasms are biphasic or triphasic diseases that are usually diagnosed in the initial ‘chronic’, ‘indolent’, or ‘stable’ phase and then spontaneously evolve after some years into an advanced phase. In patients with chronic myeloid leukaemia, the advanced phase can sometimes be subdivided into an earlier accelerated phase and a later blast phase resembling acute leukaemia. Patients with essential thrombocythaemia and polycythaemia vera transform initially to myelofibrosis and then to acute myeloid leukaemia (AML). Rarely they transform directly from the in
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Jasielec, Jagoda, and Olatoyosi Odenike. "Primary, Post-PV, and Post-ET Myelofibrosis: Clinical Features, Prognosis, and Conventional Therapy." In Contemporary Management of Myeloproliferative Neoplasms. Jaypee Brothers Medical Publishers (P) Ltd., 2015. http://dx.doi.org/10.5005/jp/books/12391_6.

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Egan, Daniel, and Jerald P. Radich. "Monitoring efforts in myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0015.

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Targeted therapy with tyrosine kinase inhibitors (TKI) has transformed the therapy of chronic myeloid leukaemia (CML), and is increasingly playing a role in the management of the myeloproliferative neoplasms (MPN), as a whole. In CML, the Philadelphia chromosome drives disease pathogenesis, and is the basis of both therapy (aimed at the BCR-ABL protein) and monitoring (the BCR-ABL chimeric mRNA). The efficacy of tyrosine kinase inhibitor therapy in CML is now accessed by reaching treatment milestones based on the BCR-ABL mRNA levels. In MPN, the landscape of genetic mutations associated with e
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Kvasnicka, Hans Michael, and Jürgen Thiele. "Haematopathology of classic myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0004.

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The classification of the World Health Organization (WHO) continues to advocate the diagnostic importance of bone marrow (BM) morphology in the diagnostic workup of myeloproliferative neoplasms (MPN). In this regard, distinctive histological BM patterns characterize specific subtypes of MPN and are the key to a meaningful clinical and molecular-defined risk stratification of patients. In this regard, the morphological denominator includes a characteristic megakaryocytic proliferation along with variable changes in the granulopoiesis and erythropoiesis. Importantly, diagnosis of MPN requires ab
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Besses, Carlos, Beatriz Bellosillo, Alberto Alvarez-Larrán, and Tariq I. Mughal. "Essential thrombocythaemia." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0010.

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Essential thrombocythaemia is a classic myeloproliferative neoplasm characterized by thrombocytosis, increased risk of thrombotic and/or haemorrhagic complications, and a trend to transformation to myelofibrosis and acute leukaemia. Mutations in JAK2, CALR, and MPL genes besides bone marrow histology are crucial elements of diagnosis. Treatment is aimed to prevent the appearance of thrombotic complications that are the main cause of morbidity and mortality. Accordingly, thrombosis risk stratification is of the utmost importance to select the appropriate treatment. Antiplatelet therapy as prima
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Hoover, Kevin B. "Lymphoproliferative and Myeloproliferative Disorders." In Musculoskeletal Imaging Volume 2, edited by Kevin B. Hoover. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190938178.003.0078.

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Chapter 78 discusses lymphoproliferative and myeloproliferative disorders, which are a disparate group of premalignant and malignant neoplasms originating in or metastasizing to the bone marrow. Included in this group of disorders is primary myelofibrosis, systemic mastocytosis, leukemia, and lymphoma. Because these tend to involve the marrow more often than the cortex, they are best detected by MRI and nuclear imaging techniques, including FDG-PET and CT. Distinguishing the disorders by imaging is often difficult because of the overlap in imaging findings. Imaging is beneficial to guide biops
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