Hematopoietic growth factors, signaling and the chronic myeloproliferative disorders

被引:11
作者
Kaushansky, Kenneth [1 ]
机构
[1] Univ Calif San Diego, Div Hematol Oncol, Dept Med, San Diego, CA 92103 USA
关键词
chronic myeloproliferative diseases; polycythemia vera; idiopathic myelofibrosis;
D O I
10.1016/j.cytogfr.2006.09.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The chronic myeloproliferative diseases (CMDs) are a group of conditions characterized by unregulated blood cell production, that due either to excessive numbers of erythrocytes, leukocytes or platelets, or their defective function cause symptoms and signs of fatigue, headache, ruddy cyanosis, hemorrhage, abdominal distension, and the complications of vascular thrombosis. In the late 19th century Vaquez provided the first description of polycythemia vera (PV) and Hueck defined idiopathic myelofibrosis (IMF). In 1920, di Guglielmo established criteria for patients with essential thrombocythemia (ET). In 195 1, Dameshek argued that these disorders, along with chronic myelogenous leukemia (CML) display many similar clinical and laboratory features [Dameshek W. Some speculations on the myeloproliferative syndromes. Blood 1951;6:372-5], and grouped them. In 2002, the World Health Organization expanded the definition of CMDs to also include chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia/hypereosinophilic syndrome (CEL/HES) and systemic mast cell disorder (SMCD) [Vardiman JW, Harris NL, Brunning RD. The World Health Organization (WHO) classification of the myeloid neoplasms. Blood 2002; 100:2292-302]. While the molecular pathogenesis of CML is well known [Melo JV, Deininger MW. Biology of chronic myelogenous leukemia-signaling pathways of initiation and transformation. Hematol Oncol Clin North Am 2004; 18:545-68], and the causes of CEL/HES and SMCD have been identified in about half of all cases [Gotlib J, Cools J, Malone III JM, Schrier SL, Gilliland DG, Coutre SE. The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management. Blood 2004;103:2879-91; Valent P, Akin C, Sperr WR, Horny HP, Metcalfe DD. Mast cell proliferative disorders: current view on variants recognized by the World Health Organization. Hematol Oncol Clin North Am 2003;17:1227-41], until very recently the etiologies of the three classically defined CMDs, PV, IMF and ET, were poorly understood. Each of these disorders is characterized by excessive hematopoiesis, a process usually dependent on one or more hematopoietic growth factors (HGFs). This review will focus on how our knowledge of the molecular mechanisms by which HGFs are produced, bind cell surface receptors and transduce survival and proliferative signals have provided the platform on which the multiple origins of CMDs can be understood and novel therapeutic interventions designed. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:423 / 430
页数:8
相关论文
共 78 条
  • [61] Hematopoietic stem and progenitor cells: Clinical and preclinical regeneration of the hematolymphoid system
    Shizuru, JA
    Negrin, RS
    Weissman, IL
    [J]. ANNUAL REVIEW OF MEDICINE, 2005, 56 : 509 - 538
  • [62] Severe defects in immunity and hematopoiesis caused by SHP-1 protein-tyrosine-phosphatase deficiency
    Shultz, LD
    Rajan, TV
    Greiner, DL
    [J]. TRENDS IN BIOTECHNOLOGY, 1997, 15 (08) : 302 - 307
  • [63] Expression of Bcl-x in erythroid precursors from patients with polycythemia vera
    Silva, M
    Richard, C
    Benito, A
    Sanz, C
    Olalla, I
    Fernández-Luna, JL
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1998, 338 (09) : 564 - 571
  • [64] PRIMARY FAMILIAL POLYCYTHEMIA - A FRAMESHIFT MUTATION IN THE ERYTHROPOIETIN RECEPTOR GENE AND INCREASED SENSITIVITY OF ERYTHROID PROGENITORS TO ERYTHROPOIETIN
    SOKOL, L
    LUHOVY, M
    GUAN, YL
    PRCHAL, JF
    SEMENZA, GL
    PRCHAL, JT
    [J]. BLOOD, 1995, 86 (01) : 15 - 22
  • [65] Blood and bone: two tissues whose fates are intertwined to create the hematopoietic stem-cell niche
    Taichman, RS
    [J]. BLOOD, 2005, 105 (07) : 2631 - 2639
  • [66] TSUI HW, 1993, NAT GENET, V4, P124, DOI 10.1038/ng0693-124
  • [67] Mast cell proliferative disorders: current view on variants recognized by the World Health Organization
    Valent, P
    Akin, C
    Sperr, WR
    Horny, HP
    Metcalfe, DD
    [J]. HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA, 2003, 17 (05) : 1227 - +
  • [68] van de Geijn GJM, 2004, REV PHYSIOL BIOCH P, V149, P53
  • [69] The World Health Organization (WHO) classification of the myeloid neoplasms
    Vardiman, JW
    Harris, NL
    Brunning, RD
    [J]. BLOOD, 2002, 100 (07) : 2292 - 2302
  • [70] Proteasomes regulate the duration of erythropoietin receptor activation by controlling down-regulation of cell surface receptors
    Verdier, F
    Walrafen, P
    Hubert, N
    Chrétien, S
    Gisselbrecht, S
    Lacombe, C
    Mayeux, P
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (24) : 18375 - 18381