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Relevant bibliographies by topics / Myeloproliferative

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Academic literature on the topic 'Myeloproliferative'

Author: Grafiati

Published: 10 March 2023

Last updated: 31 July 2025

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Journal articles on the topic "Myeloproliferative"

1

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 (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 s

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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 (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 m

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3

Gautier, Emmanuel L., Marit Westerterp, Neha Bhagwat, et al. "HDL and Glut1 inhibition reverse a hypermetabolic state in mouse models of myeloproliferative disorders." Journal of Experimental Medicine 210, no. 2 (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 shR

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Klein, Claudius, Anabel Zwick, Sandra Kissel, et al. "Ptch2 loss drives myeloproliferation and myeloproliferative neoplasm progression." Journal of Experimental Medicine 213, no. 2 (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

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Klein, Claudius, Anabel Zwick, Sandra Kissel, et al. "Ptch2 loss drives myeloproliferation and myeloproliferative neoplasm progression." Journal of Cell Biology 212, no. 3 (2016): 2123OIA11. http://dx.doi.org/10.1083/jcb.2123oia11.

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Klein, Claudius, Anabel Zwick, Sandra Kissel, et al. "Ptch2 loss drives myeloproliferation and myeloproliferative neoplasm progression." Journal of Cell Biology 212, no. 4 (2016): 2124OIA23. http://dx.doi.org/10.1083/jcb.2124oia23.

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Tripodo, Claudio, Sabina Sangaletti, Carla Guarnotta, et al. "Stromal SPARC contributes to the detrimental fibrotic changes associated with myeloproliferation whereas its deficiency favors myeloid cell expansion." Blood 120, no. 17 (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 n

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Nangalia, Jyoti, and Anthony R. Green. "Myeloproliferative neoplasms: from origins to outcomes." Hematology 2017, no. 1 (2017): 470–79. http://dx.doi.org/10.1182/asheducation-2017.1.470.

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Abstract Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations in JAK2 over a decade ago heralded a new age for patient care as a consequence of improved diagnosis and the development of therapeutic JAK inhibitors. The more recent identification of mutations in calreticulin brought with it a sense of completeness, with most patients with myeloproliferative neoplasm now having a biological basis for their excessive myeloproliferation. We are also beginning to understand the processes that lead to acquisition

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Nangalia, Jyoti, and Anthony R. Green. "Myeloproliferative neoplasms: from origins to outcomes." Blood 130, no. 23 (2017): 2475–83. http://dx.doi.org/10.1182/blood-2017-06-782037.

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Abstract Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations in JAK2 over a decade ago heralded a new age for patient care as a consequence of improved diagnosis and the development of therapeutic JAK inhibitors. The more recent identification of mutations in calreticulin brought with it a sense of completeness, with most patients with myeloproliferative neoplasm now having a biological basis for their excessive myeloproliferation. We are also beginning to understand the processes that lead to acquisition

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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 (2021): i. http://dx.doi.org/10.1016/s0889-8588(21)00010-1.

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Dissertations / Theses on the topic "Myeloproliferative"

1

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

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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 r

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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 t

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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

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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. 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. 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. 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. Baillière Tindall, 1998.

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5

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

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Petrides, Petro E., and Heike L. Pahl, eds. Molecular Basis of Chronic Myeloproliferative Disorders. 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. Springer Berlin Heidelberg, 2012.

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8

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

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9

Leukemia & Lymphoma Society of America. Coping: Support for people living with leukemia, lymphoma or myeloma. Leukemia & Lymphoma Society, 2005.

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10

D, Zanjani Esmail, Tavassoli Mehdi 1933-, Ascensao Joao L, and Wasserman Louis R, eds. Regulation of erythropoiesis. PMA Pub. Corp., 1988.

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Book chapters on the topic "Myeloproliferative"

1

Kühne, Thomas. "Myeloproliferative and Myelodysplastic/Myeloproliferative Neoplasms." In Pediatric Oncology. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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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Abraham, Soby, Bhumireddy Penchalareddy, Sumam David S., Deepu Vijayasenan, and Sridevi H B. "Identification of Myeloproliferative Neoplasms using Deep Learning." In 2024 Seventh International Women in Data Science Conference at Prince Sultan University (WiDS PSU). IEEE, 2024. http://dx.doi.org/10.1109/wids-psu61003.2024.00027.

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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). 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, et al. "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, et al. "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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Reports on the topic "Myeloproliferative"

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

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

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