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

Author: Grafiati

Published: 10 March 2023

Last updated: 31 July 2025

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1

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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Golovina, Olga G., Natalia N. Silina, Natalia E. Korsakova, and Olesya Yu Matvienko. "FUNCTIONAL ACTIVITY OF BLOOD MICROPARTICLES IN PH-NEGATIVE MYELOPROLIFERATIVE NEOPLASMS PATIENTS." Bulletin of Medical Science 34, no. 2 (2024): 6–13. http://dx.doi.org/10.31684/25418475-2024-2-6.

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Introduction. Classical Ph-negative myeloproliferative neoplasms (essential thrombocythemia, polycythemia vera, and primary myelofibrosis) are often associated with thrombotic events. Managing and preventing these complications are crucial in patient care. Blood microparticles play a role in promoting clot formation and contribute to thrombotic complications in these conditions. Objectives. This study aimed to assess the procoagulant activity of microparticles in patients with Ph-negative myeloproliferative neoplasms. Methods. A total of 141 patients were included in this study, with 57 patien

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Treaba, Diana O., Salwa Khedr, Shamlal Mangray, Cynthia Jackson, Jorge J. Castillo, and Eric S. Winer. "Acute Myeloid Leukemia Evolving from JAK 2-Positive Primary Myelofibrosis and Concomitant CD5-Negative Mantle Cell Lymphoma: A Case Report and Review of the Literature." Case Reports in Hematology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/875039.

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Primary myelofibrosis (formerly known as chronic idiopathic myelofibrosis), has the lowest incidence amongst the chronic myeloproliferative neoplasms and is characterized by a rather short median survival and a risk of progression to acute myeloid leukemia (AML) noted in a small subset of the cases, usually as a terminal event. As observed with other chronic myeloproliferative neoplasms, the bone marrow biopsy may harbor small lymphoid aggregates, often assumed reactive in nature. In our paper, we present a 70-year-old Caucasian male who was diagnosed with primary myelofibrosis, and after 8 ye

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Kiladjian, Jean-Jacques. "The spectrum of JAK2-positive myeloproliferative neoplasms." Hematology 2012, no. 1 (2012): 561–66. http://dx.doi.org/10.1182/asheducation.v2012.1.561.3807838.

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Abstract The discovery of the JAK2V617F mutation triggered an unexpected flowering of basic and clinical studies in the field of myeloproliferative neoplasms (MPNs), resulting after just a few years in an exceptional amount of new information. One important consequence of those new findings was the modification of the World Health Organization classification and diagnostic algorithms for these diseases, which is still based on the original concept developed by William Dameshek in 1951 and keeps distinct entities under the umbrella of classical Philadelphia-negative MPNs. These MPNs are essenti

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Pieri, Lisa, Paola Guglielmelli, and Alessandro Maria Vannucchi. "CHRONIC MYELOPROLIFERATIVE NEOPLASMS: A COLLABORATIVE APPROACH." Mediterranean Journal of Hematology and Infectious Diseases 2, no. 2 (2010): e2010017. http://dx.doi.org/10.4084/mjhid.2010.017.

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The classic chronic myeloproliferative neoplasms (MPN) include different entities that pose significant challenges for their optimal diagnosis, treatment and overall management. Polycythemia Vera and Essential Thrombocythemia are the most common among chronic myeloproliferative neoplasms (MPNs); major causes of morbidity and mortality are represented by arterial and venous thrombosis, as well as evolution to myelofibrosis or transformation to acute leukemia. However, survival is only minimally affected. Therapy aims at reducing the rate of thrombosis without increasing the risk of hematologic

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Daver, Naval, and Rita Assi. "An Exciting New Era in the Treatment of Myeloproliferative Neoplasms." Oncology & Hematology Review (US) 12, no. 02 (2016): 71. http://dx.doi.org/10.17925/ohr.2016.12.02.71.

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Myeloproliferative neoplasms (MPNs), including primary myelofibrosis and myelofibrosis (MF) evolving from a pre-existing MPN (post polycythemia vera- and post essential thrombocythemia-myelofibrosis) are clonal hematopoietic stem cell disorders with heterogeneous symptoms, mutational profile, transformation risk and prognosis. Given the potentially chronic disease course, the goal of therapy in MF is to alleviate associated signs and symptoms, including reduction in spleen size, weight gain, improved performance status, and control of constitutional symptoms, leading to a prolonged survival an

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Spivak, Jerry L. "Myeloproliferative Neoplasms: Challenging Dogma." Journal of Clinical Medicine 13, no. 22 (2024): 6957. http://dx.doi.org/10.3390/jcm13226957.

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Myeloproliferative neoplasms, polycythemia vera, essential thrombocytosis, and primary myelofibrosis are a unique group of clonal hematopoietic stem cell neoplasms that share somatic, gain-in-function driver mutations in JAK2, CALR, and MPL. As a consequence, these disorders exhibit similar phenotypic features, the most common of which are the ceaseless production of normal erythrocytes, myeloid cells, platelets alone or in combination, extramedullary hematopoiesis, myelofibrosis, and a potential for leukemic transformation. In the case of polycythemia vera and essential thrombocytosis, howeve

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Barbui, Tiziano, Guido Finazzi, and Anna Falanga. "Myeloproliferative neoplasms and thrombosis." Blood 122, no. 13 (2013): 2176–84. http://dx.doi.org/10.1182/blood-2013-03-460154.

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Abstract Major causes of morbidity and mortality in myeloproliferative neoplasms are represented by arterial and venous complications, progression to myelofibrosis, and transformation to acute leukemia. The pathogenesis of thrombosis results from a complex interplay of clinical and disease-related factors. Abnormalities of blood cells arising from the clonal proliferation of hematopoietic stem cells involve not only quantitative changes but also qualitative modifications that characterize the switch of these cells from a resting to a procoagulant phenotype. According to age and previous thromb

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Ristic, Slobodan, Milica Radojkovic, Tatjana Kostic, Vesna Spasovski, Sonja Pavlovic, and Vesna Cemerikic-Martinovic. "JAK2V617F mutation in a patient with B-cell chronic lymphocytic leukemia and prefibrotic primary myelofibrosis." Srpski arhiv za celokupno lekarstvo 143, no. 11-12 (2015): 739–43. http://dx.doi.org/10.2298/sarh1512739r.

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Introduction. Secondary malignancies, particularly solid tumors, are common in patients with chronic lymphocytic leukemia (CLL), but association of myeloproliferative neoplasms and chronic lymphocytic leukemia in the same patient is very rare. Case Outline. We report of a 67-year-old man with B-cell chronic lymphoid leukemia (B-CLL) who developed primary myelofibrosis (PMF) nine years after initial diagnosis. Patient received alkylation agents and purine analogue, which can be a predisposing factor for the development of myeloproliferative neoplasms. JAK2V617F mutation was not present initiall

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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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Cazzola, Mario, and Robert Kralovics. "From Janus kinase 2 to calreticulin: the clinically relevant genomic landscape of myeloproliferative neoplasms." Blood 123, no. 24 (2014): 3714–19. http://dx.doi.org/10.1182/blood-2014-03-530865.

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Abstract Our understanding of the genetic basis of myeloproliferative neoplasms began in 2005, when the JAK2 (V617F) mutation was identified in polycythemia vera, essential thrombocythemia, and primary myelofibrosis. JAK2 exon 12 and MPL exon 10 mutations were then detected in subsets of patients, and subclonal driver mutations in other genes were found to be associated with disease progression. Recently, somatic mutations in the gene CALR, encoding calreticulin, have been found in most patients with essential thrombocythemia or primary myelofibrosis with nonmutated JAK2 and MPL. The JAK-STAT

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McMullin, Mary Frances, and Lesley Ann Anderson. "Aetiology of Myeloproliferative Neoplasms." Cancers 12, no. 7 (2020): 1810. http://dx.doi.org/10.3390/cancers12071810.

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Myeloproliferative neoplasms (MPNs) have estimated annual incidence rates for polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis of 0.84, 1.03, and 0.47 per 100,000. Prevalence is much higher, particularly for PV and ET, as mortality rates are relatively low. Patients are often concerned about why they developed an MPN and epidemiological studies enable the identification of potential causative factors. Previous work in small heterogeneous studies has identified a variety of risk factors associated with MPNs including family history of MPN, autoimmune conditions,

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Melikyan, Anait L., Irina N. Subortseva, Elena A. Gilyazitdinova, et al. "Thrombosis in patients with myeloproliferative neoplasms. Case report." Terapevticheskii arkhiv 93, no. 7 (2021): 800–804. http://dx.doi.org/10.26442/00403660.2021.07.200925.

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Thrombotic complications are the most significant factors determining the prognosis in myeloproliferative neoplasms. Markers for assessing the risk of thrombosis are the number of leukocytes, platelets, hemoglobin level, hematocrit, age, molecular status, history of thrombosis, obesity, arterial hypertension, hyperlipidemia, hereditary or acquired thrombophilia. The pathogenesis of thrombosis in patients with myeloproliferative neoplasms is complex and multifactorial. In most cases, the etiological factor remains unknown. Currently, antiplatelet and anticoagulant therapy is carried out on an i

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Lanikova, Lucie, Olga Babosova, and Josef T. Prchal. "Experimental Modeling of Myeloproliferative Neoplasms." Genes 10, no. 10 (2019): 813. http://dx.doi.org/10.3390/genes10100813.

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Myeloproliferative neoplasms (MPN) are genetically very complex and heterogeneous diseases in which the acquisition of a somatic driver mutation triggers three main myeloid cytokine receptors, and phenotypically expresses as polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis (PMF). The course of the diseases may be influenced by germline predispositions, modifying mutations, their order of acquisition and environmental factors such as aging and inflammation. Deciphering these contributory elements, their mutual interrelationships, and their contribution to MPN pat

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Taj, Sadia, Mona Aziz, Maliha Asif, Amna Arooj, Madiha Islam, and Adnan Tariq. "Coagulation profile in myeloproliferative Neoplasms." Professional Medical Journal 27, no. 05 (2020): 944–49. http://dx.doi.org/10.29309/tpmj/2020.27.05.3864.

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Objectives: Evaluation of coagulation profile in patients with Myeloproliferative Neoplasms. Study Design: Cross sectional survey. Setting: Department of Haematology, Shaikh Zayed Hospital, Lahore. Period: From 10-03-2015 to 09-03-2016. Materials & Methods: A total of 55 patients of myeloproliferative neoplasms (Chronic Myeloid leukaemia, Polycythemia vera, Essential thrombocytosis and Primary Myelofibrosis) were studied over 1 year period. Patients of >15 yrs and both the genders were included. Patients already on anticoagulation and liver disease were excluded. All patients underwent

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Li, Xuedong, Mingli Xu, and Yingying Wang. "Monocyte Involvement in the Pathogenesis of Myeloproliferative Neoplasms." International Journal of Molecular Sciences 26, no. 13 (2025): 6422. https://doi.org/10.3390/ijms26136422.

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Classical BCR-ABL-negative myeloproliferative neoplasms are a heterogeneous group of hematologic malignancies, including essential thrombocythemia, polycythemia vera, and primary myelofibrosis. Monocytes, immune cells derived from hematopoietic stem cells, exhibit significant heterogeneity and contribute to immune regulation through cytokine secretion and differentiation into dendritic cells and macrophages. Aberrant monocytes are associated with the prognosis of MPNs, particularly PMF. Furthermore, these altered monocytes play a critical role in the pathogenesis and progression of MPNs. This

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Hobbs, Gabriela, Cansu Cimen Bozkus, Erin Moshier, et al. "PD-1 inhibition in advanced myeloproliferative neoplasms." Blood Advances 5, no. 23 (2021): 5086–97. http://dx.doi.org/10.1182/bloodadvances.2021005491.

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Abstract Myelofibrosis (MF) is a clonal stem cell neoplasm characterized by abnormal JAK-STAT signaling, chronic inflammation, cytopenias, and risk of transformation to acute leukemia. Despite improvements in the therapeutic options for patients with MF, allogeneic hematopoietic stem cell transplantation remains the only curative treatment. We previously demonstrated multiple immunosuppressive mechanisms in patients with MF, including increased expression of programmed cell death protein 1 (PD-1) on T cells compared with healthy controls. Therefore, we conducted a multicenter, open-label, phas

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Korsakova, N. E. "Endothelium state in Ph-negative myeloproliferative neoplasms." Сибирский научный медицинский журнал 41, no. 6 (2021): 30–44. http://dx.doi.org/10.18699/ssmj20210603.

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Thrombotic complications contribute significantly in morbidity and mortality of patients with Ph-negative myeloproliferative neoplasms (MPN) including polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Vascular endothelium is essential component of hemostatic system, and its functionality failure plays important role in prothrombotic states development. This review comprises analysis of available data on assessment of endothelium state characteristics in Ph-negative MPN and their detection with different methods. The search of literature sources was carried out using PubM

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Gul, Ayesha, Sheeba Ishtiaq, Hina Umair, and Memoona Rasheed. "Frequency of JAK2 and MPL Mutation in BCR/ABL Negative Myelofibrosis in KPK." Journal of Rawalpindi Medical College 26, no. 2 (2022): 266–70. http://dx.doi.org/10.37939/jrmc.v26i2.1845.

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Introduction: BCR-ABL1-negative myeloproliferative disorders are a sub-group of myeloproliferative neoplasms (MPNs) that consist of polycythemia Vera (PV), Essential thrombocythemia (ET) and Primary Myelofibrosis (PMF). Over the past decade, the morphological and clinical division of myeloproliferative neoplasms (MPN) has changed to a classification that describes the molecular heterogeneity and is unique to this subgroup of haematological malignancies. This includes alterations in Janus kinase 2 (JAK2), and MPL genes. Objective: To determine the frequency of JAK2 (p.V617F) and MPL (p.W515L) m

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Tamari, Roni, and Hugo Castro-Malaspina. "Allogeneic haematopoietic stem cell transplantation for primary myelofibrosis and myelofibrosis evolved from other myeloproliferative neoplasms." Current Opinion in Hematology 22, no. 2 (2015): 184–90. http://dx.doi.org/10.1097/moh.0000000000000121.

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Wang, Le, Julie Li, Leah Arbitman, et al. "Current Advances in the Diagnosis and Treatment of Major Myeloproliferative Neoplasms." Cancers 17, no. 11 (2025): 1834. https://doi.org/10.3390/cancers17111834.

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Myeloproliferative neoplasms (MPNs) are a group of rare blood cancers characterized by the excessive production of blood cells in the bone marrow. These disorders arise from acquired genetic driver mutations, with or without underlying genetic predispositions, resulting in the uncontrolled production of red blood cells, white blood cells, or platelets. The excessive cell production and abnormal signaling from driver mutations cause chronic inflammation and a higher risk of blood clots and vascular complications. The primary goals of MPN treatment are to induce remission, improve quality of lif

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Keechilat, Pavithran, and Shripad Brahmanand Pande. "Janus kinase inhibitors: jackpot or potluck?" Oncology Reviews 6, no. 1 (2012): 13. http://dx.doi.org/10.4081/oncol.2012.e13.

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The reports of a unique mutation in the Janus kinase-2 gene (<em>JAK2</em>) in polycythemia vera by several independent groups in 2005 quickly spurred the development of the Janus kinase inhibitors. In one of the great victories of translational research in recent times, the first smallmolecule Janus kinase inhibitor ruxolitinib entered a phase I trial in 2007. With the approval of ruxolitinib by the US Federal Drug Administration in November 2011 for high-risk and intermediate-2 risk myelofibrosis, a change in paradigm has occurred in the management of a subset of myeloproliferati

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Toros, Ahmet Burak, Serkan Gokcay, Guven Cetin, Muhlis Cem Ar, Yesim Karagoz, and Besir Kesici. "Portal Hypertension and Myeloproliferative Neoplasms: A Relationship Revealed." ISRN Hematology 2013 (September 16, 2013): 1–5. http://dx.doi.org/10.1155/2013/673781.

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Background/Objectives. Patients with myeloproliferative neoplasms have a well-established increased risk of thrombosis. Many trials report identification of an underlying myeloproliferative neoplasm by investigation of the patients developing portal hypertensive esophagus and/or fundus variceal hemorrhage in the absence of any known etiology. This trial was designed to investigate the association between myeloproliferative neoplasms and portal hypertension and to detect the frequency of portal hypertension development in this subset of patients. Methodology. Twenty-nine patients previously dia

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Giraldo-Rincon, Ana Isabel, Sara Naranjo Molina, Natalia Gomez-Lopera, et al. "JAK2, CALR, and MPL Mutation Profiles in Colombian patients with BCR-ABL Negative Myeloproliferative Neoplasms." Colombia Medica 54, no. 3 (2023): e2035353. http://dx.doi.org/10.25100/cm.v54i3.5353.

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BackgroundAmong the chronic myeloproliferative neoplasms (MPNs) not associated with BCR-ABL mutations are polycythemia vera, primary myelofibrosis, and essential thrombocythemia. These diseases are caused by gene mutations, such as the JAK2, MPL, and CALR genes, which regulate the JAK-STAT signaling pathway. ObjectiveThis study aimed to establish the frequencies of mutations in the JAK2, MPL, and CALR genes in Colombian patients with a negative clinical diagnosis of BCR-ABL chronic myeloproliferative neoplasms. MethodsThe JAK2 V617F and MPL W515K mutations and deletions or insertions in exon 9

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Torres, Dania G., Jhemerson Paes, Allyson G. da Costa, et al. "JAK2 Variant Signaling: Genetic, Hematologic and Immune Implication in Chronic Myeloproliferative Neoplasms." Biomolecules 12, no. 2 (2022): 291. http://dx.doi.org/10.3390/biom12020291.

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The JAK2V617F variant constitutes a genetic alteration of higher frequency in BCR/ABL1 negative chronic myeloproliferative neoplasms, which is caused by a substitution of a G ˃ T at position 1849 and results in the substitution of valine with phenylalanine at codon 617 of the polypeptide chain. Clinical, morphological and molecular genetic features define the diagnosis criteria of polycythemia vera, essential thrombocythemia and primary myelofibrosis. Currently, JAK2V617F is associated with clonal hematopoiesis, genomic instability, dysregulations in hemostasis and immune response. JAK2V617F c

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Tanashyan, Мarine М., Polina I. Kuznetsova, Anton A. Raskurazhev, et al. "Clinical and Neuroimaging Patterns of Ischemic Stroke in Ph-negative Myeloproliferative Neoplasms." Annals of Clinical and Experimental Neurology 18, no. 3 (2024): 14–25. http://dx.doi.org/10.17816/acen.1164.

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Introduction. Philadelphia-negative myeloproliferative neoplasms (MPNs) are a rare blood disorder characterized by pancytosis and thrombohemorrhagic complications. The aim of this article is to describe clinical and neuroimaging patterns of brain changes in patients with MPN. Materials and methods. The study included 152 patients with an established diagnosis of MPN (according to WHO criteria 2008, 2016). A clinical and neurological examination, laboratory tests, and magnetic resonance imaging of the brain were performed. Results. In patients with polycythemia vera and primary myelofibrosis, n

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Rumi, Elisa, and Mario Cazzola. "Diagnosis, risk stratification, and response evaluation in classical myeloproliferative neoplasms." Blood 129, no. 6 (2017): 680–92. http://dx.doi.org/10.1182/blood-2016-10-695957.

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Abstract Philadelphia-negative classical myeloproliferative neoplasms (MPNs) include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The 2016 revision of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues includes new criteria for the diagnosis of these disorders. Somatic mutations in the 3 driver genes, that is, JAK2, CALR, and MPL, represent major diagnostic criteria in combination with hematologic and morphological abnormalities. PV is characterized by erythrocytosis with suppressed endogenous erythropoietin production, bone mar

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Iurlo, Alessandra, Daniele Cattaneo, and Umberto Gianelli. "Blast Transformation in Myeloproliferative Neoplasms: Risk Factors, Biological Findings, and Targeted Therapeutic Options." International Journal of Molecular Sciences 20, no. 8 (2019): 1839. http://dx.doi.org/10.3390/ijms20081839.

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Myeloproliferative neoplasms represent a heterogenous group of disorders of the hematopoietic stem cell, with an intrinsic risk of evolution into acute myeloid leukemia. The frequency of leukemic evolution varies according to myeloproliferative neoplasms subtype. It is highest in primary myelofibrosis, where it is estimated to be approximately 10–20% at 10 years, following by polycythemia vera, with a risk of 2.3% at 10 years and 7.9% at 20 years. In essential thrombocythemia, however, transformation to acute myeloid leukemia is considered relatively uncommon. Different factors are associated

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Atere, Muhammed, Rana Al-Zakhari, Jennifer Collins, Francesco Rotatori, and Lloyd Muzangwa. "Atypical Myocardial Infarction with Apical Thrombus and Systemic Embolism: A Rare Presentation of Likely JAK2 V617F-Positive Myeloproliferative Neoplasm." Case Reports in Oncological Medicine 2020 (May 19, 2020): 1–4. http://dx.doi.org/10.1155/2020/9654048.

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A few types of myeloproliferative neoplasms may be significant for Janus-associated kinase 2 mutation, JAK2 V617F, including polycythemia vera, essential thrombocythemia, and primary myelofibrosis. The prevalence of JAK2 mutation is low in the general population but higher in patients with myeloproliferative neoplasms. Some patients with JAK2 V617F-positive essential thrombocythemia are asymptomatic, but others may develop hemorrhagic or thromboembolic complications. Thromboembolism may occur in vessels of high flow organs like the heart and, thereby, present as myocardial infarction. Nonethel

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Prakash, Sonam, and Attilio Orazi. "How I Diagnose Primary Myelofibrosis." American Journal of Clinical Pathology 157, no. 4 (2022): 518–30. http://dx.doi.org/10.1093/ajcp/aqac016.

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Abstract Objectives Primary myelofibrosis (PMF) is a BCR/ABL1-negative myeloproliferative neoplasm (MPN) with a shorter overall survival and a higher leukemic transformation than other BCR/ABL1-negative MPNs. Diagnosis of PMF can be challenging given its clinical, morphologic, molecular overlap with other myeloid neoplasms also associated with myelofibrosis, and reactive conditions. Methods We summarize and discuss the clinical, morphologic, and molecular features useful for diagnosing PMF as well as salient features helpful in distinguishing PMF from myelodysplastic syndrome with associated f

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Langabeer, Stephen E., James Nolan, Karl Haslam, Lindsey Clarke, Richard Flavin, and Eibhlin Conneally. "Evading Capture by Residual Disease Monitoring: Extramedullary Manifestation ofJAK2V617F-Positive Primary Myelofibrosis After Allogeneic Stem Cell Transplantation." Case Reports in Hematology 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/703457.

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Monitoring of theJAK2V617F allele burden in myeloproliferative neoplasms after allogeneic stem cell transplantation is useful to determine levels of residual disease and has the potential to detect early relapse and guide subsequent clinical intervention. A case is described of aJAK2V617F-positive primary myelofibrosis patient who underwent allogeneic stem cell transplantation. Prospective residual disease monitoring of the peripheral blood failed to detect an extramedullary manifestation of the disease, a periorbital myeloid sarcoma, arising nearly three years after transplant. This case serv

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Vargas-Viveros, Pablo, Rafael Hurtado Monroy, and Myrna Candelaria-Hernandez. "Significant Improvement In Quality Of Life (QoL) In Patients With Chronic Myeloproliferative Neoplasms and Myelofibrosis Treated With JAK-1 and JAK-2 Inhibitor Ruxolitinib. A Single Institution Experience In Mexico." Blood 122, no. 21 (2013): 5252. http://dx.doi.org/10.1182/blood.v122.21.5252.5252.

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Abstract Introduction Myeloproliferative Neoplasms can shorten the life of patients and affect severely their quality of life as a result of constitutional symptoms mediated by cytokines and from massive splenomegaly characteristic of these diseases. The objective measurement of symptoms in Myelofibrosis is essential for the presence of general constitutional symptoms as fatigue and is considered adverse prognostic value for survival. The systematic measurement of symptoms in Myelofibrosis is essential for assessing the outcome of treatment with JAK-2 inhibitors. Material and Methods To assess

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Sghibneva-Bobeico, Nina, Vasile Musteata, Maria Robu, et al. "Clinical patterns and complete blood count parameters in the young patients with primary myelofibrosis in the prefibrotic stage." Moldovan Journal of Health Sciences, no. 4 (December 2022): 22–26. http://dx.doi.org/10.52645/mjhs.2022.4.04.

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Introduction. Primary myelofibrosis is a rare myeloproliferative neoplasm that affects 0.2-1.5 people per 100,000. As a rule, the diagnosis is confirmed after 60 years, but recently, hematologists around the world have encountered the problem of primary myelofibrosis in young people. The classic manifestations of myelofibrosis are characterized by splenomegaly, cytopenia, and bone marrow fibrosis, but in patients younger than 40 years, the diagnosis is most often made in the prefibrotic stage of the neoplasm. The aim of the paper is to identify and evaluate the clinical and hematological featu

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Simon, Zsófia, Imelda Marton, Zita Borbényi, and Árpád Illés. "Aktualitások a primer myelofibrosis ellátásában." Orvosi Hetilap 157, no. 39 (2016): 1547–56. http://dx.doi.org/10.1556/650.2016.30531.

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Primary myelofibrosis is one of the Philadelphia negative chronic myeloproliferative neoplasms. It is a rare disease featured by cytopenias and hepatosplenomegaly. Although the etiology of the disease is still unknown, our knowledge about its pathology and prognosis has been improving in the last few years. Furthermore, the JAK2 inhibitor ruxolitinib has become available in Hungary since 2015. Beside its high efficacy in spleen volume and in reduction of myelofibrosis-associated symptoms, this novel therapy also exerts a disease-modifying effect and, therefore, ruxolitinib may improve the life

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Koschmieder, Steffen. "How I Manage Thrombotic/Thromboembolic Complications in Myeloproliferative Neoplasms." Hämostaseologie 40, no. 01 (2020): 047–53. http://dx.doi.org/10.1055/s-0040-1701474.

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AbstractPatients with myeloproliferative neoplasms (MPNs), such as polycythemia vera, essential thrombocythemia, and primary myelofibrosis, are at increased risk for arterial and venous thrombosis/thromboembolism. In particular, the risk of splanchnic venous thrombosis, such as portal vein thrombosis or Budd–Chiari syndrome, is significantly higher in patients with MPN than in the normal population. At the same time, MPN patients are at increased risk for severe bleeding. Therefore, the treatment of patients with MPN must be based on their suspected probability of thrombosis/thromboembolism an

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Dasanu, Constantin A. "Erythematous skin lesions with necrotic centers on lower extremities due to the use of ruxolitinib for primary myelofibrosis." Journal of Oncology Pharmacy Practice 25, no. 4 (2018): 990–92. http://dx.doi.org/10.1177/1078155218768875.

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Ruxolitinib is a small molecule JAK-2 inhibitor approved for the treatment of certain myeloproliferative neoplasms. Ruxolitinib-related skin toxicity is extremely rare. We report herein an unusual erythematous skin eruption with necrotic centers involving lower extremities in a patient with primary myelofibrosis treated with ruxolitinib. Awareness of this unusual skin toxicity with ruxolitinib becomes even more important as JAK-2 inhibition might soon find clinical applications in dermatology.

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Arachchillage, Deepa RJ, and Mike Laffan. "Pathogenesis and Management of Thrombotic Disease in Myeloproliferative Neoplasms." Seminars in Thrombosis and Hemostasis 45, no. 06 (2019): 604–11. http://dx.doi.org/10.1055/s-0039-1693477.

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AbstractChronic myeloproliferative neoplasms (MPN) are characterized by clonal expansion of an abnormal hematopoietic stem/progenitor cell and include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Venous thrombosis, often at unusual sites, including splanchnic vein thrombosis and arterial thrombosis, as well as a hemorrhagic tendency and a propensity to transform into myelofibrosis or acute leukemia are common complications in patients with MPNs. The pathogenesis of thrombosis in MPN patients is complex and multifactorial. Disease related factors, suc

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Sabattini, Elena, Marco Pizzi, Claudio Agostinelli, et al. "Progression in Ph-Chromosome-Negative Myeloproliferative Neoplasms: An Overview on Pathologic Issues and Molecular Determinants." Cancers 13, no. 21 (2021): 5531. http://dx.doi.org/10.3390/cancers13215531.

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Progression in Ph-chromosome-negative myeloproliferative neoplasms (MPN) develops with variable incidence and time sequence in essential thrombocythemia, polycythemia vera, and primary myelofibrosis. These diseases show different clinic-pathologic features and outcomes despite sharing deregulated JAK/STAT signaling due to mutations in either the Janus kinase 2 or myeloproliferative leukemia or CALReticulin genes, which are the primary drivers of the diseases, as well as defined diagnostic criteria and biomarkers in most cases. Progression is defined by the development or worsening of marrow fi

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Gulbay, Gonca, Elif Yesilada, Mehmet Ali Erkurt, Harika Gozukara Bag, Irfan Kuku, and Emin Kaya. "Evaluation of the JAK2 V617F gene mutation in myeloproliferative neoplasms cases: a one-center study from Eastern Anatolia." Turkish Journal of Biochemistry 44, no. 4 (2019): 492–98. http://dx.doi.org/10.1515/tjb-2018-0054.

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AbstractObjectiveDetection ofJAK2V617F in myeloproliferative neoplasms (MPNs) is very important in both diagnosis and disease progression. In our study, we investigated the frequency ofJAK2V617F mutation in patients with myeloproliferative disorders.MethodsWe retrospectively reviewed the records of 720 patients (174 females and 546 males) who were tested for JAK2 V617F mutation from January 2007 to December 2017.ResultsIn our patients were determined 22.6%JAK2V617F mutation. 33.3% in women, 19.2% in men have been positive forJAK2V617F mutation. In our studyJAK2V617F present in 48.6% of essenti

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Koschmieder, Steffen. "The Approach to Thrombosis Prevention across the Spectrum of Philadelphia-Negative Classic Myeloproliferative Neoplasms." Hemato 2, no. 3 (2021): 392–402. http://dx.doi.org/10.3390/hemato2030025.

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Patients with myeloproliferative neoplasm (MPN) are potentially facing diminished life expectancy and decreased quality of life, due to thromboembolic and hemorrhagic complications, progression to myelofibrosis or acute leukemia with ensuing signs of hematopoietic insufficiency, and disturbing symptoms such as pruritus, night sweats, and bone pain. In patients with essential thrombocythemia (ET) or polycythemia vera (PV), current guidelines recommend both primary and secondary measures to prevent thrombosis. These include acetylsalicylic acid (ASA) for patients with intermediate- or high-risk

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Belčič Mikič, Tanja, Tadej Pajič, Samo Zver, and Matjaž Sever. "The Contemporary Approach to CALR-Positive Myeloproliferative Neoplasms." International Journal of Molecular Sciences 22, no. 7 (2021): 3371. http://dx.doi.org/10.3390/ijms22073371.

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CALR mutations are a revolutionary discovery and represent an important hallmark of myeloproliferative neoplasms (MPN), especially essential thrombocythemia and primary myelofibrosis. To date, several CALR mutations were identified, with only frameshift mutations linked to the diseased phenotype. It is of diagnostic and prognostic importance to properly define the type of CALR mutation and subclassify it according to its structural similarities to the classical mutations, a 52-bp deletion (type 1 mutation) and a 5-bp insertion (type 2 mutation), using a statistical approximation algorithm (AGA

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