Relevant bibliographies by topics / Myeloproliferative

Academic literature on the topic 'Myeloproliferative'

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Published: 10 March 2023

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Journal articles on the topic "Myeloproliferative"

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Morgan, R., F. Hecht, ML Cleary, J. Sklar, and MP Link. "Leukemia with Down's syndrome: translocation between chromosomes 1 and 19 in acute myelomonocytic leukemia following transient congenital myeloproliferative syndrome." Blood 66, no. 6 (December 1, 1985): 1466–68. http://dx.doi.org/10.1182/blood.v66.6.1466.1466.

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Abstract A girl with Down's syndrome was born with a myeloproliferative disorder. The child had spontaneous regression of the myeloproliferation, with acute leukemia developing at a later date. Morphologic, cytochemical, immunologic, and immunoglobulin gene configuration studies all supported the diagnosis of acute nonlymphocytic leukemia. High-resolution chromosome studies revealed that the leukemic cells consistently contained a translocation between chromosomes 1 and 19: der(19)t(1;19)(q25;p13). Spontaneous regression of the transient myeloproliferative syndrome of the newborn with Down's syndrome may not always be permanent, and the transient myeloproliferative syndrome may sometimes represent an early sign of acute nonlymphocytic leukemia.
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Morgan, R., F. Hecht, ML Cleary, J. Sklar, and MP Link. "Leukemia with Down's syndrome: translocation between chromosomes 1 and 19 in acute myelomonocytic leukemia following transient congenital myeloproliferative syndrome." Blood 66, no. 6 (December 1, 1985): 1466–68. http://dx.doi.org/10.1182/blood.v66.6.1466.bloodjournal6661466.

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A girl with Down's syndrome was born with a myeloproliferative disorder. The child had spontaneous regression of the myeloproliferation, with acute leukemia developing at a later date. Morphologic, cytochemical, immunologic, and immunoglobulin gene configuration studies all supported the diagnosis of acute nonlymphocytic leukemia. High-resolution chromosome studies revealed that the leukemic cells consistently contained a translocation between chromosomes 1 and 19: der(19)t(1;19)(q25;p13). Spontaneous regression of the transient myeloproliferative syndrome of the newborn with Down's syndrome may not always be permanent, and the transient myeloproliferative syndrome may sometimes represent an early sign of acute nonlymphocytic leukemia.
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Klein, Claudius, Anabel Zwick, Sandra Kissel, Christine Ulrike Forster, Dietmar Pfeifer, Marie Follo, Anna Lena Illert, et al. "Ptch2 loss drives myeloproliferation and myeloproliferative neoplasm progression." Journal of Experimental Medicine 213, no. 2 (February 1, 2016): 273–90. http://dx.doi.org/10.1084/jem.20150556.

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JAK2V617F+ myeloproliferative neoplasms (MPNs) frequently progress into leukemias, but the factors driving this process are not understood. Here, we find excess Hedgehog (HH) ligand secretion and loss of PTCH2 in myeloproliferative disease, which drives canonical and noncanonical HH-signaling. Interestingly, Ptch2−/− mice mimic dual pathway activation and develop a MPN-phenotype with leukocytosis (neutrophils and monocytes), strong progenitor and LKS mobilization, splenomegaly, anemia, and loss of lymphoid lineages. HSCs exhibit increased cell cycling with improved stress hematopoiesis after 5-FU treatment, and this results in HSC exhaustion over time. Cytopenias, LKS loss, and mobilization are all caused by loss of Ptch2 in the niche, whereas hematopoietic loss of Ptch2 drives leukocytosis and promotes LKS maintenance and replating capacity in vitro. Ptch2−/− niche cells show hyperactive noncanonical HH signaling, resulting in reduced production of essential HSC regulators (Scf, Cxcl12, and Jag1) and depletion of osteoblasts. Interestingly, Ptch2 loss in either the niche or in hematopoietic cells dramatically accelerated human JAK2V617F-driven pathogenesis, causing transformation of nonlethal chronic MPNs into aggressive lethal leukemias with >30% blasts in the peripheral blood. Our findings suggest HH ligand inhibitors as possible drug candidates that act on hematopoiesis and the niche to prevent transformation of MPNs into leukemias.
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Klein, Claudius, Anabel Zwick, Sandra Kissel, Christine Ulrike Forster, Dietmar Pfeifer, Marie Follo, Anna Lena Illert, et al. "Ptch2 loss drives myeloproliferation and myeloproliferative neoplasm progression." Journal of Cell Biology 212, no. 3 (February 1, 2016): 2123OIA11. http://dx.doi.org/10.1083/jcb.2123oia11.

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Klein, Claudius, Anabel Zwick, Sandra Kissel, Christine Ulrike Forster, Dietmar Pfeifer, Marie Follo, Anna Lena Illert, et al. "Ptch2 loss drives myeloproliferation and myeloproliferative neoplasm progression." Journal of Cell Biology 212, no. 4 (February 15, 2016): 2124OIA23. http://dx.doi.org/10.1083/jcb.2124oia23.

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Gautier, Emmanuel L., Marit Westerterp, Neha Bhagwat, Serge Cremers, Alan Shih, Omar Abdel-Wahab, Dieter Lütjohann, et al. "HDL and Glut1 inhibition reverse a hypermetabolic state in mouse models of myeloproliferative disorders." Journal of Experimental Medicine 210, no. 2 (January 14, 2013): 339–53. http://dx.doi.org/10.1084/jem.20121357.

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A high metabolic rate in myeloproliferative disorders is a common complication of neoplasms, but the underlying mechanisms are incompletely understood. Using three different mouse models of myeloproliferative disorders, including mice with defective cholesterol efflux pathways and two models based on expression of human leukemia disease alleles, we uncovered a mechanism by which proliferating and inflammatory myeloid cells take up and oxidize glucose during the feeding period, contributing to energy dissipation and subsequent loss of adipose mass. In vivo, lentiviral inhibition of Glut1 by shRNA prevented myeloproliferation and adipose tissue loss in mice with defective cholesterol efflux pathway in leukocytes. Thus, Glut1 was necessary to sustain proliferation and potentially divert glucose from fat storage. We also showed that overexpression of the human ApoA-I transgene to raise high-density lipoprotein (HDL) levels decreased Glut1 expression, dampened myeloproliferation, and prevented fat loss. These experiments suggest that inhibition of Glut-1 and HDL cholesterol–raising therapies could provide novel therapeutic approaches to treat the energy imbalance observed in myeloproliferative disorders.
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Tripodo, Claudio, Sabina Sangaletti, Carla Guarnotta, Pier P. Piccaluga, Matilde Cacciatore, Michela Giuliano, Giovanni Franco, et al. "Stromal SPARC contributes to the detrimental fibrotic changes associated with myeloproliferation whereas its deficiency favors myeloid cell expansion." Blood 120, no. 17 (October 25, 2012): 3541–54. http://dx.doi.org/10.1182/blood-2011-12-398537.

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Abstract In myeloid malignancies, the neoplastic clone outgrows normal hematopoietic cells toward BM failure. This event is also sustained by detrimental stromal changes, such as BM fibrosis and osteosclerosis, whose occurrence is harbinger of a dismal prognosis. We show that the matricellular protein SPARC contributes to the BM stromal response to myeloproliferation. The degree of SPARC expression in BM stromal elements, including CD146+ mesenchymal stromal cells, correlates with the degree of stromal changes, and the severity of BM failure characterizing the prototypical myeloproliferative neoplasm primary myelofibrosis. Using Sparc−/− mice and BM chimeras, we demonstrate that SPARC contributes to the development of significant stromal fibrosis in a model of thrombopoietin-induced myelofibrosis. We found that SPARC deficiency in the radioresistant BM stroma compartment impairs myelofibrosis but, at the same time, associates with an enhanced reactive myeloproliferative response to thrombopoietin. The link betwen SPARC stromal deficiency and enhanced myeloid cell expansion under a myeloproliferative spur is also supported by the myeloproliferative phenotype resulting from the transplantation of defective Apcmin mutant hematopoietic cells into Sparc−/− but not WT recipient BM stroma. Our results highlight a complex influence of SPARC over the stromal and hematopoietic BM response in myeloproliferative conditions.
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Čermák, Jaroslav. "Mixed myelodysplastic/myeloproliferative syndromes." Onkologie 10, no. 3 (June 1, 2016): 127–30. http://dx.doi.org/10.36290/xon.2016.027.

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Hoffman, Ronald, Ross Levine, John Mascarenhas, and Raajit K. Rampal. "Myeloproliferative Neoplasms." Hematology/Oncology Clinics of North America 35, no. 2 (April 2021): i. http://dx.doi.org/10.1016/s0889-8588(21)00010-1.

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Harrison, Claire N., and Sarah A. Bassiony. "Myeloproliferative neoplasms." Medicine 49, no. 5 (May 2021): 269–73. http://dx.doi.org/10.1016/j.mpmed.2021.02.003.

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Dissertations / Theses on the topic "Myeloproliferative"

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Zetterberg, Eva. "Angiogenesis in myeloproliferative disorders /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-383-3/.

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Shihab-El-Deen, Awatef. "Clonal development in myeloproliferative disorders." Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72055.

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We assessed clonal development and extent of progression of hemopoietic malignancies (dysmyelopoietic syndrome (DMPS) and acute myelogenous leukemia) by examining in vitro growth patterns of their normal and leukemic progenitors. Additional phenotypic and cytogenetic analysis of an in vitro human myeloid leukemia model (HL-60) and its variant sublines were performed. These were aimed at determining cytogenetic abnormalities associated with phenotypic changes which accompany the derivation of these variant sublines. Our findings indicate that in vitro bone marrow cultures can be used clinically to rule out preleukemia, and that quantitations of bone marrow culture (CFU-C) can determine the potential for the development of acute leukemia in the DMPS patients. Acute leukemia developed in 48% of DMPS patients with a median transformation of 10 months.
In acute leukemia, there was a preferential growth of normal karyotype in the in vitro cultures even among the phenotypically specified "blast" colonies.
Analysis of HL-60 variant sublines demonstrated the development of specific chromosomal abnormalities (1q+, iso8q, iso17q) in two cell lines (clones resistant to chemical induction) in association with loss of differentiation. These specific chromosomal abnormalities are known to be associated with tumor progression. The development of 1q+ abnormality was associated with loss of myeloperoxidase reaction and persistence of primary granules in that specific variant. A group of variant subclones was also associated with loss of differentiation, cytogenetically however, they demonstrated a revert to near diploid near normal karyotypes.
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Singh, Rathna. "Genomic diversity in myeloproliferative neoplasms." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/12268.

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An exploratory study on the genetics of primary myelofibrosis was undertaken on the peripheral blood of 42 consecutive patients. Results of cytogenetic studies showed success rates with peripheral blood were superior to corresponding bone marrow analysis(P<0.001) and was preferred for ongoing patient monitoring. Several novel findings were detected in the study: A novel group of polyploid cases strongly associated with the gain of chromosome 1q was detected and showed a trend toward advancing disease. Further investigation of polyploid cases showed copy number gain around the pericentromeric region (P=0.02). One sample studied further showed unequal cell division in daughter nuclei, loss of chromosomal material from cells via micronuclei and failure of chromosome separation at mitosis. This provided some evidence of genetic instability and a pathogenic mechanism for the polyploidy. A subset of independent cases showed somatic mosaicism for copy number gain of the MAPT/KANSL1 locus on chromosome 17q21.31, involved commonly with neurodevelopmental defects. Other regions containing neurodevelopmental genes pertain to the NF1 locus on 17q11.2 suggestive of a role in aging and cancer development. The profile of DNA aberrations detected by SNP array confirmed similarities to t-MDS/AML and CN-LOH occurred commonly in regions associated with DNA repair. In addition massively parallel targeted sequencing complemented cytogenetic studies in detecting known mutations in MPN.
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Macdonald, Donald Hugh Charles. "Chromosome 13 abnormalities in myeloproliferative diseases." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411308.

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Basu, Titiksha [Verfasser], and Heike L. [Akademischer Betreuer] Pahl. "Myeloproliferative neoplasms: cause, mechanism and treatment." Freiburg : Universität, 2017. http://d-nb.info/1162443340/34.

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Jones, Amy Victoria. "The molecular pathogenesis of myeloproliferative neoplasms." Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/162665/.

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Myeloproliferative neoplasms (MPNs) are a heterogeneous group of haematological stem cell malignancies characterised by proliferation of one or more cells of the myeloid lineage. The molecular investigation of MPN was revolutionized in 2005 by the finding that approximately 95% of cases with polycythaemia vera (PV) and 50-60% of cases of essential thrombocythaemia (ET) and primary myelofibrosis (PMF) are characterised by a single acquired mutation, JAK2 V617F. My study has focused on four principal areas: (i) Involvement of V617F in other myeloid disorders. After developing sensitive methods to detect and quantify V617F, this mutation was identified in 17% of cases of atypical chronic myeloid leukaemia (17/99) as well as other atypical MPN, thus demonstrating that it was more widely involved in myeloid disorders that initially thought. Homozygosity of V617F was shown to have arisen by acquired uniparental disomy (UPD) and examination of two cases with V617F plus either KIT D816V or BCR-ABL demonstrated that the mutations had arisen in independent clones. (ii) In vitro assays to predict imatinib sensitivity. Haemopoietic colony and liquid cultures were used to determine if peripheral blood or bone marrow cells from atypical MPN cases (n=200) were sensitive to imatinib. Of those that responded in one or both cultures (n=185) some had known abnormalities of PDGFRA or PDGFRB, but a significant minority proved negative for all molecular tests suggesting the presence of uncharacterised imatinib-sensitive mutations. (iii) V617F as a marker of response to therapy. JAK2 V617F was used as a molecular marker to monitor the response of PV patients (n=21) to therapy with imatinib and interferon-α. Neither therapy eradicated V617F but there was a modest reduction in %V617F which correlated with haematological response. By contrast, in those patients that did not respond (n=13) the %V617F marginally increased. (iv) Genetic predisposition to MPN. Whilst investigating the possible contribution of JAK2 single nucleotide polymorphisms to the phenotypic diversity associated with V617F, marked skewing of alleles associated with the mutation was observed. Further investigation revealed that V617Fassociated disease is strongly associated with a specific constitutional JAK2 haplotype, designated 46/1, in all three disease entities compared to healthy controls (PV, n=192, P=2.9x10-16; ET, n=78, P=8.2x10-9 and MF, n=41, P=8.0x10-5). Furthermore, allele-specific PCR demonstrated that V617F specifically arises on the 46/1 allele in most cases. The 46/1 JAK2 haplotype thus predisposes to the development of V617F associated MPNs (OR=3.7; 95% CI 3.1-4.3) and provides a model whereby a constitutional genetic factor is associated with an increased risk of acquiring a specific somatic mutation.
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`Arnold, Claire. "Intracellular signalling pathways in myeloproliferative neoplasms." Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680884.

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Lynch, Susan Fraser. "Platelet and vascular studies in myeloproliferative disorders." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/24860.

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We have studied a cohort of patients with polycythaemia vera (PV) primary thrombocythaemia (PT) and primary myelofibrosis (PMF) and described their clinical and laboratory features in comparison to other published observations. The demographic, haematological and molecular characteristics of our cohort were similar to other retrospective analyses, but the occurrence of thrombo-haemorrhagic complications was lower. The presence of vascular abnormalities in these patients was investigated using both established markers and an assay was devised to measure platelet, endothelial, leucocytes and red cell microparticles in platelet poor plasma using flow cytometry techniques. This assay was optimised for pre-analytical variables, the most important of which was found to be sample centrifugation. In keeping with previous studies, increased platelet activation was observed in PV and PT patients compared to healthy controls using both established markers and as evidenced by increased numbers of platelet microparticles. There was no evidence of endothelial disturbance using the soluble endothelial marker E-selectin but we did observe elevated endothelial microparticles in patients compared to controls. Microparticles may therefore be useful as a marker of vascular abnormalities in these disorders and in view of their prothrombotic properties may be an additional pathogenic mechanism in the prothrombotic state and a potential therapeutic target. In relation to bone marrow fibrosis, plasma levels of platelet α-granule contents, including the pro-fibrotic cytokine transforming growth factor β (TGFβ), were studied. We observed elevated levels of TGFβ in patients compared to controls, with the highest levels in patients with PMF and in those with PT or PV who had more marked fibrosis. Further, levels of TGFβ were strongly associated with another α-granule protein beta-thromboglobulin, suggesting that platelet α-granules may be an important source for this pro-fibrotic cytokine.
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Boyd, M. T. "Detection of retroviral indicators in myeloproliferative diseases." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234379.

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Vassiliou, George Steliou. "The molecular pathogenesis of the myeloproliferative disorders." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614681.

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Books on the topic "Myeloproliferative"

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Melo, Junia V., and John M. Goldman. Myeloproliferative Disorders. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-34506-0.

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Verstovsek, Srdan, and Ayalew Tefferi, eds. Myeloproliferative Neoplasms. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-266-7.

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Barbui, Tiziano, and Ayalew Tefferi, eds. Myeloproliferative Neoplasms. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-24989-1.

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Richard, Green A., and Pearson Tom C, eds. Myeloproliferative disorders. London: Baillière Tindall, 1998.

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Mesa, Ruben A., and Claire Harrison, eds. Managing Myeloproliferative Neoplasms. Cambridge: Cambridge University Press, 2016. http://dx.doi.org/10.1017/cbo9781316017852.

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Myeloproliferative neoplasms: Biology and therapy. New York: Humana Press, 2011.

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Petrides, Petro E., and Heike L. Pahl, eds. Molecular Basis of Chronic Myeloproliferative Disorders. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18738-4.

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Barbui, Tiziano. Myeloproliferative Neoplasms: Critical Concepts and Management. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012.

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Parker, James N., and Philip M. Parker. The official patient's sourcebook on myeloproliferative disorders. San Diego, Calif: Icon Health Publications, 2002.

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Dallinger, Kenneth James Charles. Myeloproliferative disorders: The effect on (1) fibrinogen turnover, (2) prostanoid metabolism. Birmingham: University of Birmingham, 1987.

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Book chapters on the topic "Myeloproliferative"

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Kühne, Thomas. "Myeloproliferative and Myelodysplastic/Myeloproliferative Neoplasms." In Pediatric Oncology, 43–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-20359-6_5.

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Bueso-Ramos, Carlos E., and James W. Vardiman. "Diagnosis and Classification of the BCR-ABL1-Negative Myeloproliferative Neoplasms." In Myeloproliferative Neoplasms, 1–37. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_1.

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Gotlib, Jason. "Eosinophilic Disorders: Differential Diagnosis and Management." In Myeloproliferative Neoplasms, 181–203. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_10.

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Pardanani, Animesh, and Ayalew Tefferi. "Pathogenesis, Diagnosis, Classification, and Management of Systemic Mastocytosis." In Myeloproliferative Neoplasms, 205–21. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_11.

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Abdel-Wahab, Omar, and Ross L. Levine. "Genetics of the Myeloproliferative Neoplasms." In Myeloproliferative Neoplasms, 39–68. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_2.

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Reilly, John T. "Cytogenetic Findings in Classical MPNs." In Myeloproliferative Neoplasms, 69–83. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_3.

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Cervantes, Francisco, and Juan-Carlos Hernández-Boluda. "Prognostic Factors in Classic Myeloproliferative Neoplasms." In Myeloproliferative Neoplasms, 85–96. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_4.

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Finazzi, Guido, and Tiziano Barbui. "Therapy of Polycythemia Vera and Essential Thrombocythemia." In Myeloproliferative Neoplasms, 97–115. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_5.

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Barosi, Giovanni. "Conventional and Investigational Therapy for Primary Myelofibrosis." In Myeloproliferative Neoplasms, 117–38. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_6.

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Kerbauy, Daniella M. B., and H. Joachim Deeg. "Hematopoietic Cell Transplantation for Myelofibrosis." In Myeloproliferative Neoplasms, 139–50. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-266-7_7.

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Conference papers on the topic "Myeloproliferative"

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Paratte, G., G. Domenighetti, and H. Stricker. "Pulmonary Hypertension (PH) Associated with Myeloproliferative Diseases." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4924.

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Chauhan, S., Y. Galan, S. Tripathi, V. Gidwani, and H. Amin. "Association of Pulmonary Hypertension and Myeloproliferative Disorders." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1962.

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Rita Anggraini, Dwi, Hidayat Hidayat, and Mega Sitorus. "Identification of JAK2V617F Mutation on Myeloproliferative Disorders in Medan." In 1st Public Health International Conference (PHICo 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/phico-16.2017.65.

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Hlaing, K. M., S. Gaballa, and B. B. Patel. "Platelets Gone Wild a Rare Complication of Myeloproliferative Disorders." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1743.

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Parada-Turska, J., B. Sokolowska, A. Walter-Croneck, A. Dmoszynska, L. Szczepanski, J. Brzozowska, M. Sledzinska, and M. Kokoszka. "AB0219 Quantitative hemostatic indices in secondary and myeloproliferative thrombocytosis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.740.

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Feng-Feng Wang, Lawrence WC Chan, SP Yip, and Benjamin YM Yung. "MicroRNA-mediated alteration of TET2 interaction network in myeloproliferative neoplasms." In 2011 IEEE 13th International Conference on e-Health Networking, Applications and Services (Healthcom 2011). IEEE, 2011. http://dx.doi.org/10.1109/health.2011.6026756.

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Scaldaferri, M., A. Varese, M. Tonelli, D. Barilà, A. Bianco, G. Valinotti, E. Caiazza, D. Martinetto, M. Ferroni, and F. Cattel. "CP-100 Pegylated interferon ALFA 2-A in myeloproliferative neoplasms." In 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.99.

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Gorthi, R., and J. K. Mwangi. "Riociguat for Treatment of Chronic Myeloproliferative Disorder Associated Pulmonary Hypertension." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7244.

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Migura, Anthony M., Mary Beth Beasley, and Timothy J. Harkin. "Myeloproliferative Involvement Of The Lung: An Unusual Manifestation Of Myelofibrosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5662.

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Mazzucato, M., M. G. Del Ben, A. Casonato, V. De Angelis, and L. De Marco. "PLATELET MEMBRANE GLYCOPROTEINS ABNORMALITIES IN MYELOPROLIFERATIVE DISORDERS. STRUCTURE/FUNCTION RELATIONSHIP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643508.

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The platelet membrane glycoproteins (GP) lb and GPIIb/IIIa were investigated in 10 patients with myeloproliferative disorders. 2 patients had essential thrombocytemia (ET), 2 had chronic myeloid leukemia (CML) and 6 policytemia vera (PV). The number of GP molecules were detected by radiolabelled monoclonal antibodies anti GPIb and anti GPIIb/IIIa complex (gift of dr. Z.M. Ruggeri) and their function was evaluated by using, in a binding assay, purified radiolabelled asialo von Willebrand factor (1251 ASvWF) and purified radiolabelled fibrinogen (1251 F). Binding isotherms were evaluated by Scatchard type analysis using the computer assisted programLigand. The binding of 1251 anti GPIb to the platelets of the ten patients showed 14,955 ∓ 4,636 molecules/platelet (M/Plt) compared to 19,790 ∓ 3,791 M/Plt of 11 normals with a p value < 0.01. The binding of 125IAsvWF to the GPIb of nonstimulated platelets in platelet rich plasma (PRP) was then measured and ound to be decreased. The dissociation constants (Kds) were within normal values except in one patient. There was a good correlation (r = 0.91, p < 0.01) between the amount of 1251 ASvWF bound and GPIb molecules. The binding of radiolabelled anti GPIIb/IIIa to the platelets of six patients (4 with PV and 2 with CML) was measured and found to be constantly decreased in all patients with a mean value of 25,349 ∓ 2,077 M/Plt compared to 43,192 ∓ 6,354 M/Plt found in normals (p < 0.01). 1251 fibrinogen binding to the GPIIb/IIIa complex of ADP + adrenalin stimulated washed platelet was studied in 2 patients and we found 16,267 M/Plt and 14,752 M/Plt respectively, significantly diminished when compared to the mean value of 36,591 M/Plt found in 2 normal controls. The Kds were within normal values. Our studies demonstrate a significant decrease of GPIb and GPIIb/IIIa on the platelet membrane of patients with myeloproliferative disorders. Furthermore this decrease is accompanied by a diminished binding of both vWF and F to their platelets receptors. These findings may partly explain the hemorragic tendency often encountered in these patients.
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Reports on the topic "Myeloproliferative"

1

Reuther, Gary W. Enhancing Targeted Therapy for Myeloproliferative Neoplasms. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada613864.

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2

Reuther, Gary W. Enhancing Targeted Therapy for Myeloproliferative Neoplasms. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada600492.

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