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Articles de revues sur le sujet « Myeloproliferative »

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Auteur : Grafiati
Publié le 10 mars 2023

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1

Morgan, R., F. Hecht, ML Cleary, J. Sklar et 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 (1 décembre 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 et 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 (1 décembre 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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3

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 (1 février 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 (1 février 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 (15 février 2016) : 2124OIA23. http://dx.doi.org/10.1083/jcb.2124oia23.

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6

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 (14 janvier 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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7

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 (25 octobre 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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8

Čermák, Jaroslav. « Mixed myelodysplastic/myeloproliferative syndromes ». Onkologie 10, no 3 (1 juin 2016) : 127–30. http://dx.doi.org/10.36290/xon.2016.027.

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9

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

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10

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

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11

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

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12

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

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13

Costa Villela, Neysimelia, Gustavo Zamperlini, Patrícia Shimoda Ikeuti, Roseane Vasconcelos Gouveia, Simone De Castro Resende Franco et Luiz Fernando Lopes. « Myeloproliferative neoplasms ». JOURNAL OF BONE MARROW TRANSPLANTATION AND CELLULAR THERAPY 2, no 4 (30 novembre 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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14

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

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15

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

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16

Murray, Jim. « Myeloproliferative disorders ». Clinical Medicine 5, no 4 (1 juillet 2005) : 328–32. http://dx.doi.org/10.7861/clinmedicine.5-4-328.

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17

Bick, Rodger L., et W. Robert Laughlin. « Myeloproliferative Syndromes ». Laboratory Medicine 24, no 12 (1 décembre 1993) : 770–76. http://dx.doi.org/10.1093/labmed/24.12.770.

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18

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

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19

Messinezy, Maria, et 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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20

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

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21

Liput, Joseph, Daniel A. Smith, Rose Beck et 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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22

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

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23

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

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24

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

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25

Levine, Ross L., et D. Gary Gilliland. « Myeloproliferative disorders ». Blood 112, no 6 (15 septembre 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 JAK2V617F− MPD, suggesting that constitutive activation of this signaling pathway is a unifying feature of these disorders. Although the discovery of mutations in the JAK-STAT pathway is important from a pathogenetic and diagnostic perspective, important questions remain regarding the role of this single disease allele in 3 related but clinically distinct disorders, and the role of additional genetic events in MPD disease pathogenesis. In addition, these observations provide a foundation for development of small molecule inhibitors of JAK2 that are currently being tested in clinical trials. This review will discuss our understanding of the pathogenesis of PV, ET, and PMF, the potential role of JAK2-targeted therapy, and the important unanswered questions that need to be addressed to improve clinical outcome.
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26

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

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27

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

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28

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

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29

Hussein, K., G. Büsche, J. Schlue, U. Lehmann et H. Kreipe. « Myeloproliferative Neoplasien ». Der Pathologe 33, no 6 (21 octobre 2012) : 508–17. http://dx.doi.org/10.1007/s00292-012-1651-3.

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

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31

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

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32

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

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33

Binder et Fehr. « Myeloproliferative Syndrome ». Therapeutische Umschau 61, no 2 (1 février 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, Essentiellen Thrombozythämie und Chronisch Idiopathischen Myelofibrose diskutiert.
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Bench, Anthony J., Nicholas C. P. Cross, Brian J. P. Huntly, Elisabeth P. Nacheva et Anthony R. Green. « Myeloproliferative disorders ». Best Practice & ; Research Clinical Haematology 14, no 3 (septembre 2001) : 531–51. http://dx.doi.org/10.1053/beha.2001.0153.

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35

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

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36

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

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37

Nangalia, Jyoti, et Anthony R. Green. « Myeloproliferative neoplasms : from origins to outcomes ». Hematology 2017, no 1 (8 décembre 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 of somatic mutations and the factors that influence subsequent clonal expansion and emergence of disease. Extended genomic profiling has established a multitude of additional acquired mutations, particularly prevalent in myelofibrosis, where their presence carries prognostic implications. A major goal is to integrate genetic, clinical, and laboratory features to identify patients who share disease biology and clinical outcome, such that therapies, both existing and novel, can be better targeted.
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38

Nangalia, Jyoti, et Anthony R. Green. « Myeloproliferative neoplasms : from origins to outcomes ». Blood 130, no 23 (7 décembre 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 of somatic mutations and the factors that influence subsequent clonal expansion and emergence of disease. Extended genomic profiling has established a multitude of additional acquired mutations, particularly prevalent in myelofibrosis, where their presence carries prognostic implications. A major goal is to integrate genetic, clinical, and laboratory features to identify patients who share disease biology and clinical outcome, such that therapies, both existing and novel, can be better targeted.
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39

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

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41

Orazi, A., et U. Germing. « The myelodysplastic/myeloproliferative neoplasms : myeloproliferative diseases with dysplastic features ». Leukemia 22, no 7 (15 mai 2008) : 1308–19. http://dx.doi.org/10.1038/leu.2008.119.

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

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

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Subortseva, I. N., et A. I. Melikyan. « MYELODYSPLASTIC/MYELOPROLIFERATIVE DISEASES ». Oncohematology 11, no 4 (1 janvier 2016) : 8–17. http://dx.doi.org/10.17650/1818-8346-2016-11-4-8-17.

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

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46

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

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47

Campbell, Peter J., et Anthony R. Green. « The Myeloproliferative Disorders ». New England Journal of Medicine 355, no 23 (7 décembre 2006) : 2452–66. http://dx.doi.org/10.1056/nejmra063728.

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48

Griesshammer, M., et K. Döhner. « Chronische myeloproliferative Neoplasien ». DMW - Deutsche Medizinische Wochenschrift 139, no 06 (28 janvier 2014) : 243–46. http://dx.doi.org/10.1055/s-0033-1359988.

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49

Spivak, Jerry L., Giovanni Barosi, Gianni Tognoni, Tiziano Barbui, Guido Finazzi, Roberto Marchioli et Monia Marchetti. « Chronic Myeloproliferative Disorders ». Hematology 2003, no 1 (1 janvier 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 difficult. In Section I, Dr. Jerry Spivak introduces current clinical controversies involving the CMPD, in particular the diagnostic challenges. Two new molecular assays may prove useful in the diagnosis and classification of CMPD. In 2000, the overexpression in PV granulocytes of the mRNA for the neutrophil antigen NBI/CD177, a member of the uPAR/Ly6/CD59 family of plasma membrane proteins, was documented. Overexpression of PRV-1 mRNA appeared to be specific for PV since it was not observed in secondary erythrocytosis. At this time, it appears that overexpression of granulocyte PRV-1 in the presence of an elevated red cell mass supports a diagnosis of PV; absence of PRV-1 expression, however, should not be grounds for excluding PV as a diagnostic possibility. Impaired expression of Mpl, the receptor for thrombopoietin, in platelets and megakaryocytes has been first described in PV, but it has also been observed in some patients with ET and IMF. The biologic basis appears to be either alternative splicing of Mpl mRNA or a single nucleotide polymorphism, both of which involve Mpl exon 2 and both of which lead to impaired posttranslational glycosylation and a dominant negative effect on normal Mpl expression. To date, no Mpl DNA structural abnormality or mutation has been identified in PV, ET or IMF. In Section II, Dr. Tiziano Barbui reviews the best clinical evidence for treatment strategy design in PV and ET. Current recommendations for cytoreductive therapy in PV are still largely similar to those at the end of the PVSG era. Phlebotomy to reduce the red cell mass and keep it at a safe level (hematocrit < 45%) remains the cornerstone of treatment. Venesection is an effective and safe therapy and previous concerns about potential side effects, including severe iron deficiency and an increased tendency to thrombosis or myelofibrosis, were erroneous. Many patients require no other therapy for many years. For others, however, poor compliance to phlebotomy or progressive myeloproliferation, as indicated by increasing splenomegaly or very high leukocyte or platelet counts, may call for the introduction of cytoreductive drugs. In ET, the therapeutic trade-off between reducing thrombotic events and increasing the risk of leukemia with the use of cytoreductive drugs should be approached by patient risk stratification. Thrombotic deaths seem very rare in low-risk ET subjects and there are no data indicating that fatalities can be prevented by starting cytoreductive drugs early. Therefore, withholding chemotherapy might be justifiable in young, asymptomatic ET patients with a platelet count below 1,500,000/mm3 and with no additional risk factors for thrombosis. If cardiovascular risk factors together with ET are identified (smoking, obesity, hypertension, hyperlipidemia) it is wise to consider platelet-lowering agents on an individual basis. In Section III, Dr. Gianni Tognoni discusses the role of aspirin therapy in PV based on the recently completed European Collaboration on Low-dose Aspirin in Polycythemia Vera (ECLAP) Study, a multi-country, multicenter project aimed at describing the natural history of PV as well as the efficacy of low-dose aspirin. Aspirin treatment lowered the risk of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke (relative risk 0.41 [95% CI 0.15–1.15], P = .0912). Total and cardiovascular mortality were also reduced by 46% and 59%, respectively. Major bleedings were slightly increased nonsignificantly by aspirin (relative risk 1.62, 95% CI 0.27–9.71). In Section IV, Dr. Giovanni Barosi reviews our current understanding of the pathophysiology of IMF and, in particular, the contributions of anomalous megakaryocyte proliferation, neoangiogenesis and abnormal CD34+ stem cell trafficking to disease pathogenesis. The role of newer therapies, such as low-conditioning stem cell transplantation and thalidomide, is discussed in the context of a general treatment strategy for IMF. The results of a Phase II trial of low-dose thalidomide as a single agent in 63 patients with myelofibrosis with meloid metaplasia (MMM) using a dose-escalation design and an overall low dose of the drug (The European Collaboration on MMM) will be presented. Considering only patients who completed 4 weeks of treatment, 31% had a response: this was mostly due to a beneficial effect of thalidomide on patients with transfusion dependent anemia, 39% of whom abolished transfusions, patients with moderate to severe thrombocytopenia, 28% of whom increased their platelet count by more than 50 × 109/L, and patients with the largest splenomegalies, 42% of whom reduced spleen size of more than 2 cm.
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Koschmieder, Steffen, et Tim H. Brümmendorf. « Myeloproliferative Neoplasien (MPN) ». Der Klinikarzt 47, no 09 (septembre 2018) : 398–402. http://dx.doi.org/10.1055/a-0686-5746.

Texte intégral
Résumé :
ZusammenfassungMyeloproliferative Neoplasien (MPN) sind klonale Stammzellerkrankungen, die typischerweise mit der Vemehrung einer oder mehrerer Blutzellreihen, einer Knochenmarkhyperplasie und einer (Hepato)-Splenomegalie als Zeichen der extramedullären Hämatopoese einhergehen. Gefürchtete Komplikationen der MPN sind Thromboembolien und schwergradige Blutungen, eine Knochenmarkverfaserung (Myelofibrose) mit konsekutiver hämatopoetischer Insuffizienz sowie der Übergang in eine akute Leukämie. Man unterscheidet die 4 klassischen MPN (Chronische Myeloische Leukämie [CML], Polycythämia vera [PV], Essentielle Thrombozythämie [ET], Primäre Myelofibrose [PMF]) von den nicht-klassischen MPN (Chronische Eosinophilen-Leukämie [CEL], Chronische Neutrophilen-Leukämie [CNL] und MPN-unklassifizierbar [MPN-U]). Sowohl der Verlauf der Erkrankungen als auch deren Symptomatik sind sehr heterogen, und eine exakte Diagnosestellung ist wichtig für die adäquate Einschätzung der Prognose und für die Beratung und Behandlung der betroffenen Patienten. Zur Diagnostik gehören neben Anamnese und ausführlicher körperlicher Untersuchung die Erhebung von Blutbild und Differenzialblutbild, eine Knochenmarkuntersuchung (Zytologie, Histologie, Chromosomenanalyse) sowie die molekulargenetische Untersuchung des peripheren Blutes (je nach MPN-Subtyp Bcr-Abl- oder Fip1L1-PDGFRA-Transkripte, JAK2617F-, CALR- und MPL-Mutationen, CSF3R- und SETBP1-Mutationen, etc). Differenzialdiagnostisch müssen u. a. die systemische Mastoztyose und die MDS/MPN-Overlap-Syndrome von den MPN abgegrenzt werden. Die Therapie ist abhängig von der Prognose der Erkrankung (Abschätzung durch verschiedene Prognose-Scores) und reicht von „Watchful waiting“ über Aderlässe, Thrombozytenaggregationshemmung und Antikoagulation bis hin zur medikamentösen Zytoreduktion, Entzündungshemmung und allogenen Stammzelltransplantation. Die Diagnose und Therapieweichenstellung gehört in die Hände des erfahrenen Spezialisten, und vor Therapiebeginn sollten dem Patienten die Teilnahme an Bioregistern und klinischen Studien erläutert werden. Informationen hierzu sind über die „German Study Group for MPN“ (GSG-MPN) erhältlich (https://www.cto-im3.de/gsgmpn/).
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