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Journal articles on the topic 'Myeloproliferative'

Author: Grafiati

Published: 10 March 2023

Last updated: 31 July 2025

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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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2

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

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

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12

Publicover, Amy, and Patrick Medd. "Myeloproliferative neoplasms." Clinical Medicine 13, no. 2 (2013): 188–92. http://dx.doi.org/10.7861/clinmedicine.13-2-188.

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13

Kiladjian, Jean-Jacques. "Myeloproliferative neoplasms." HemaSphere 2 (June 2018): 138. http://dx.doi.org/10.1097/hs9.0000000000000099.

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14

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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15

Wilkins, Bridget S. "Myeloproliferative neoplasms." Diagnostic Histopathology 27, no. 9 (2021): 373–79. http://dx.doi.org/10.1016/j.mpdhp.2021.06.003.

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16

Spivak, Jerry L. "Myeloproliferative Neoplasms." New England Journal of Medicine 376, no. 22 (2017): 2168–81. http://dx.doi.org/10.1056/nejmra1406186.

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17

Murray, Jim. "Myeloproliferative disorders." Clinical Medicine 5, no. 4 (2005): 328–32. http://dx.doi.org/10.7861/clinmedicine.5-4-328.

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18

Bick, Rodger L., and W. Robert Laughlin. "Myeloproliferative Syndromes." Laboratory Medicine 24, no. 12 (1993): 770–76. http://dx.doi.org/10.1093/labmed/24.12.770.

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19

Cross, Nick. "Myeloproliferative neoplasms." HemaSphere 3 (June 2019): 141. http://dx.doi.org/10.1097/hs9.0000000000000263.

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20

Messinezy, Maria, and T. C. Pearson. "Myeloproliferative Disorders." Medicine 28, no. 3 (2000): 50–55. http://dx.doi.org/10.1383/medc.28.3.50.28361.

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21

Harrison, Claire N. "Myeloproliferative disorders." Medicine 32, no. 6 (2004): 58–60. http://dx.doi.org/10.1383/medc.32.6.58.36664.

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22

Liput, Joseph, Daniel A. Smith, Rose Beck, and Nikhil H. Ramaiya. "Myeloproliferative Neoplasms." Journal of Computer Assisted Tomography 43, no. 4 (2019): 652–63. http://dx.doi.org/10.1097/rct.0000000000000893.

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23

Harrison, Claire N., and Susan E. Robinson. "Myeloproliferative disorders." Medicine 37, no. 4 (2009): 183–85. http://dx.doi.org/10.1016/j.mpmed.2008.12.006.

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24

Harrison, Claire N., and Clodagh Keohane. "Myeloproliferative neoplasms." Medicine 41, no. 5 (2013): 265–68. http://dx.doi.org/10.1016/j.mpmed.2013.03.005.

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25

Harrison, Claire N., and Joe S. Lee. "Myeloproliferative neoplasms." Medicine 45, no. 5 (2017): 275–79. http://dx.doi.org/10.1016/j.mpmed.2017.02.013.

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26

Levine, Ross L., and D. Gary Gilliland. "Myeloproliferative disorders." Blood 112, no. 6 (2008): 2190–98. http://dx.doi.org/10.1182/blood-2008-03-077966.

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Abstract In 1951 William Dameshek classified polycythemia vera (PV), essential thombocytosis (ET), and primary myelofibrosis (PMF) as pathogenetically related myeloproliferative disorders (MPD). Subsequent studies demonstrated that PV, ET, and PMF are clonal disorders of multipotent hematopoietic progenitors. In 2005, a somatic activating mutation in the JAK2 nonreceptor tyrosine kinase (JAK2V617F) was identified in most patients with PV and in a significant proportion of patients with ET and PMF. Subsequent studies identified additional mutations in the JAK-STAT pathway in some patients with

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27

Gilbert, Harriet S. "Myeloproliferative Disorders." Clinics in Geriatric Medicine 1, no. 4 (1985): 773–93. http://dx.doi.org/10.1016/s0749-0690(18)30911-x.

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28

Lange, T., T. Kiefer, C. Junghanss, C. Wickenhauser, T. Ernst, and F. Heidel. "Myeloproliferative Neoplasien." best practice onkologie 7, no. 5 (2012): 34–44. http://dx.doi.org/10.1007/s11654-012-0411-4.

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29

Schmitt, Karla, Susanne Isfort, Steffen Koschmieder, and Tim H. Brümmendorf. "Myeloproliferative Neoplasien." best practice onkologie 10, no. 5 (2015): 46–57. http://dx.doi.org/10.1007/s11654-015-0245-y.

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30

Hussein, K., G. Büsche, J. Schlue, U. Lehmann, and H. Kreipe. "Myeloproliferative Neoplasien." Der Pathologe 33, no. 6 (2012): 508–17. http://dx.doi.org/10.1007/s00292-012-1651-3.

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31

Kim, Julie, Rami Y. Haddad, and Ehab Atallah. "Myeloproliferative Neoplasms." Disease-a-Month 58, no. 4 (2012): 177–94. http://dx.doi.org/10.1016/j.disamonth.2012.01.002.

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32

Meier, Brian, and John H. Burton. "Myeloproliferative Disorders." Emergency Medicine Clinics of North America 32, no. 3 (2014): 597–612. http://dx.doi.org/10.1016/j.emc.2014.04.014.

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33

Young, Karen M. "Myeloproliferative Disorders." Veterinary Clinics of North America: Small Animal Practice 15, no. 4 (1985): 769–81. http://dx.doi.org/10.1016/s0195-5616(85)50035-2.

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34

Binder and Fehr. "Myeloproliferative Syndrome." Therapeutische Umschau 61, no. 2 (2004): 131–42. http://dx.doi.org/10.1024/0040-5930.61.2.131.

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Myeloproliferative Syndrome sind hämatopoietische Stammzellerkrankungen, die zur autonomen Proliferation einer oder mehrer Blutzellreihen führen. Sie werden wegen gemeinsamer klinischer und hämatologischer Merkmale, ihrer klonalen Hämatopoiese und der genetischen Instabilität mit unterschiedlicher Transformationstendenz in eine akute Leukämie als Gruppe verwandter hämatopoietischer Neoplasien zusammengefasst. In der vorliegenden Übersicht werden relevante Aspekte der klinischen Präsentation und Prognose, sowie aktuelle diagnostische und therapeutische Maßnahmen der Polycythaemia vera, Essentie

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35

Bench, Anthony J., Nicholas C. P. Cross, Brian J. P. Huntly, Elisabeth P. Nacheva, and Anthony R. Green. "Myeloproliferative disorders." Best Practice & Research Clinical Haematology 14, no. 3 (2001): 531–51. http://dx.doi.org/10.1053/beha.2001.0153.

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36

Tefferi, Ayalew, and Animesh Pardanani. "Myeloproliferative Neoplasms." JAMA Oncology 1, no. 1 (2015): 97. http://dx.doi.org/10.1001/jamaoncol.2015.89.

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37

Meier, Brian, and John H. Burton. "Myeloproliferative Disorders." Hematology/Oncology Clinics of North America 31, no. 6 (2017): 1029–44. http://dx.doi.org/10.1016/j.hoc.2017.08.007.

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38

Čermák, Jaroslav. "Mixed myelodysplastic/myeloproliferative syndromes." Onkologie 10, no. 3 (2016): 127–30. http://dx.doi.org/10.36290/xon.2016.027.

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39

Itoyama, Shinji, and Yoshitake Hayashi. "Myeloproliferative disorder of rats induced by myeloproliferative sarcoma virus." Keio Journal of Medicine 36, no. 1 (1987): 74–80. http://dx.doi.org/10.2302/kjm.36.74.

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40

Vardiman, James W. "Myelodysplastic syndromes, chronic myeloproliferative diseases, and myelodysplastic/myeloproliferative diseases." Seminars in Diagnostic Pathology 20, no. 3 (2003): 154–79. http://dx.doi.org/10.1016/s0740-2570(03)00025-x.

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41

Orazi, A., and U. Germing. "The myelodysplastic/myeloproliferative neoplasms: myeloproliferative diseases with dysplastic features." Leukemia 22, no. 7 (2008): 1308–19. http://dx.doi.org/10.1038/leu.2008.119.

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42

Klion, Amy D., Pierre Noel, Cem Akin, et al. "Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness." Blood 101, no. 12 (2003): 4660–66. http://dx.doi.org/10.1182/blood-2003-01-0006.

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Abstract Since serum tryptase levels are elevated in some patients with myeloproliferative disorders, we examined their utility in identifying a subset of patients with hypereosinophilic syndrome (HES) and an underlying myeloproliferative disorder. Elevated serum tryptase levels (&gt; 11.5 ng/mL) were present in 9 of 15 patients with HES and were associated with other markers of myeloproliferation, including elevated B12 levels and splenomegaly. Although bone marrow biopsies in these patients showed increased numbers of CD25+ mast cells and atypical spindle-shaped mast cells, patients with

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43

H. Dunphy, Cherie. "Myelodysplastic/Myeloproliferative Neoplasms." Current Cancer Therapy Reviews 8, no. 1 (2012): 52–65. http://dx.doi.org/10.2174/157339412799462530.

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44

El-Sharkawy, Farah, and Elizabeth Margolskee. "Pediatric Myeloproliferative Neoplasms." Clinics in Laboratory Medicine 41, no. 3 (2021): 529–40. http://dx.doi.org/10.1016/j.cll.2021.04.010.

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45

Subortseva, I. N., and A. I. Melikyan. "MYELODYSPLASTIC/MYELOPROLIFERATIVE DISEASES." Oncohematology 11, no. 4 (2016): 8–17. http://dx.doi.org/10.17650/1818-8346-2016-11-4-8-17.

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46

Malcovati, L., and M. Cazzola. "Myelodysplastic/myeloproliferative disorders." Haematologica 93, no. 1 (2008): 4–6. http://dx.doi.org/10.3324/haematol.11374.

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47

Skoda, R. C. "Hereditary myeloproliferative disorders." Haematologica 95, no. 1 (2010): 6–8. http://dx.doi.org/10.3324/haematol.2009.015941.

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48

Campbell, Peter J., and Anthony R. Green. "The Myeloproliferative Disorders." New England Journal of Medicine 355, no. 23 (2006): 2452–66. http://dx.doi.org/10.1056/nejmra063728.

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49

Griesshammer, M., and K. Döhner. "Chronische myeloproliferative Neoplasien." DMW - Deutsche Medizinische Wochenschrift 139, no. 06 (2014): 243–46. http://dx.doi.org/10.1055/s-0033-1359988.

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50

Spivak, Jerry L., Giovanni Barosi, Gianni Tognoni, et al. "Chronic Myeloproliferative Disorders." Hematology 2003, no. 1 (2003): 200–224. http://dx.doi.org/10.1182/asheducation-2003.1.200.

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Abstract The Philadelphia chromosome-negative chronic myeloproliferative disorders (CMPD), polycythemia vera (PV), essential thrombocythemia (ET) and chronic idiopathic myelofibrosis (IMF), have overlapping clinical features but exhibit different natural histories and different therapeutic requirements. Phenotypic mimicry amongst these disorders and between them and nonclonal hematopoietic disorders, lack of clonal diagnostic markers, lack of understanding of their molecular basis and paucity of controlled, prospective therapeutic trials have made the diagnosis and management of PV, ET and IMF

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