CoChat
Sign Up
Cited by 616

The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.

Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms

Vainchenker, William, Kralovics, Robert·2017·Blood
DOI 10.1182/blood-2016-10-695940
Open this paper in CoChat — free account

Abstract

The genetic landscape of classical myeloproliferative neoplasm (MPN) is in large part elucidated. The MPN-restricted driver mutations, including those in JAK2, calreticulin (CALR), and myeloproliferative leukemia virus (MPL), abnormally activate the cytokine receptor/JAK2 pathway and their downstream effectors, more particularly the STATs. The most frequent mutation, JAK2V617F, activates the 3 main myeloid cytokine receptors (erythropoietin receptor, granulocyte colony-stimulating factor receptor, and MPL) whereas CALR or MPL mutants are restricted to MPL activation. This explains why JAK2V617F is associated with polycythemia vera, essential thrombocythemia (ET), and primary myelofibrosis (PMF) whereas CALR and MPL mutants are found in ET and PMF. Other mutations in genes involved in epigenetic regulation, splicing, and signaling cooperate with the 3 MPN drivers and play a key role in the PMF pathogenesis. Mutations in epigenetic regulators TET2 and DNMT3A are involved in disease initiation and may precede the acquisition of JAK2V617F. Other mutations in epigenetic regulators such as EZH2 and ASXL1 also play a role in disease initiation and disease progression. Mutations in the splicing machinery are predominantly found in PMF and are implicated in the development of anemia or pancytopenia. Both heterogeneity of classical MPNs and prognosis are determined by a specific genomic landscape, that is, type of MPN driver mutations, association with other mutations, and their order of acquisition. However, factors other than somatic mutations play an important role in disease initiation as well as disease progression such as germ line predisposition, inflammation, and aging. Delineation of these environmental factors will be important to better understand the precise pathogenesis of MPN.

Overview

Integrity signals

Registry

Crossref · 10.1182/blood-2016-10-695940

Cites

12 of 12 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Research works printed but not linked: 114

  1. Spivak, 2004, The chronic myeloproliferative disorders: clonality and clinical heterogeneity, Semin Hematol, 41, 1, 10.1053/j.seminhematol.2004.02.011 · DOI
  2. Barbui, 2011, Survival and disease progression in essential thrombocythemia are significantly influenced by accurate morphologic diagnosis: an international study, J Clin Oncol, 29, 3179, 10.1200/JCO.2010.34.5298 · DOI
  3. James, 2005, A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera, Nature, 434, 1144, 10.1038/nature03546 · DOI
  4. Kralovics, 2005, A gain-of-function mutation of JAK2 in myeloproliferative disorders, N Engl J Med, 352, 1779, 10.1056/NEJMoa051113 · DOI · Paper page
  5. Levine, 2005, Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis, Cancer Cell, 7, 387, 10.1016/j.ccr.2005.03.023 · DOI · Paper page
  6. Baxter, 2005, Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders, Lancet, 365, 1054, 10.1016/S0140-6736(05)71142-9 · DOI · Paper page
  7. Kralovics, 2002, Acquired uniparental disomy of chromosome 9p is a frequent stem cell defect in polycythemia vera, Exp Hematol, 30, 229, 10.1016/S0301-472X(01)00789-5 · DOI
  8. Sozer, 2009, The presence of JAK2V617F mutation in the liver endothelial cells of patients with Budd-Chiari syndrome, Blood, 113, 5246, 10.1182/blood-2008-11-191544 · DOI
  9. Rumi, 2014, JAK2 or CALR mutation status defines subtypes of essential thrombocythemia with substantially different clinical course and outcomes, Blood, 123, 1544, 10.1182/blood-2013-11-539098 · DOI
  10. Szpurka, 2006, Refractory anemia with ringed sideroblasts associated with marked thrombocytosis (RARS-T), another myeloproliferative condition characterized by JAK2 V617F mutation, Blood, 108, 2173, 10.1182/blood-2006-02-005751 · DOI
  11. Levine, 2005, The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia, Blood, 106, 3377, 10.1182/blood-2005-05-1898 · DOI
  12. Hinds, 2016, Germ line variants predispose to both JAK2 V617F clonal hematopoiesis and myeloproliferative neoplasms, Blood, 128, 1121, 10.1182/blood-2015-06-652941 · DOI · Paper page
  13. Hirsch, 2016, Clonal history of a cord blood donor cell leukemia with prenatal somatic JAK2 V617F mutation, Leukemia, 30, 1756, 10.1038/leu.2016.31 · DOI
  14. Steensma, 2015, Clonal hematopoiesis of indeterminate potential and its distinction from myelodysplastic syndromes, Blood, 126, 9, 10.1182/blood-2015-03-631747 · DOI · Paper page
  15. Scott, 2007, JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis, N Engl J Med, 356, 459, 10.1056/NEJMoa065202 · DOI
  16. Passamonti, 2011, Molecular and clinical features of the myeloproliferative neoplasm associated with JAK2 exon 12 mutations, Blood, 117, 2813, 10.1182/blood-2010-11-316810 · DOI
  17. Pikman, 2006, MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia, PLoS Med, 3, e270, 10.1371/journal.pmed.0030270 · DOI
  18. Defour, 2016, Oncogenic activation of MPL/thrombopoietin receptor by 17 mutations at W515: implications for myeloproliferative neoplasms, Leukemia, 30, 1214, 10.1038/leu.2015.271 · DOI
  19. Rumi, 2013, Acquired copy-neutral loss of heterozygosity of chromosome 1p as a molecular event associated with marrow fibrosis in MPL-mutated myeloproliferative neoplasms, Blood, 121, 4388, 10.1182/blood-2013-02-486050 · DOI
  20. Beer, 2008, MPL mutations in myeloproliferative disorders: analysis of the PT-1 cohort, Blood, 112, 141, 10.1182/blood-2008-01-131664 · DOI
  21. Chaligné, 2007, Evidence for MPL W515L/K mutations in hematopoietic stem cells in primitive myelofibrosis, Blood, 110, 3735, 10.1182/blood-2007-05-089003 · DOI
  22. Malcovati, 2009, Molecular and clinical features of refractory anemia with ringed sideroblasts associated with marked thrombocytosis, Blood, 114, 3538, 10.1182/blood-2009-05-222331 · DOI
  23. Ding, 2004, Familial essential thrombocythemia associated with a dominant-positive activating mutation of the c-MPL gene, which encodes for the receptor for thrombopoietin, Blood, 103, 4198, 10.1182/blood-2003-10-3471 · DOI
  24. Cabagnols, 2016, Presence of atypical thrombopoietin receptor (MPL) mutations in triple-negative essential thrombocythemia patients, Blood, 127, 333, 10.1182/blood-2015-07-661983 · DOI
  25. Milosevic Feenstra, 2016, Whole-exome sequencing identifies novel MPL and JAK2 mutations in triple-negative myeloproliferative neoplasms, Blood, 127, 325, 10.1182/blood-2015-07-661835 · DOI
  26. Pietra, 2016, Differential clinical effects of different mutation subtypes in CALR-mutant myeloproliferative neoplasms, Leukemia, 30, 431, 10.1038/leu.2015.277 · DOI
  27. Cabagnols, 2015, Differential association of calreticulin type 1 and type 2 mutations with myelofibrosis and essential thrombocytemia: relevance for disease evolution, Leukemia, 29, 249, 10.1038/leu.2014.270 · DOI
  28. Broséus, 2014, Presence of calreticulin mutations in JAK2-negative polycythemia vera, Blood, 124, 3964, 10.1182/blood-2014-06-583161 · DOI · Paper page
  29. Theocharides, 2016, Homozygous calreticulin mutations in patients with myelofibrosis lead to acquired myeloperoxidase deficiency, Blood, 127, 3253, 10.1182/blood-2016-02-696310 · DOI
  30. Szuber, Novel germline mutations in the calreticulin gene: implications for the diagnosis of myeloproliferative neoplasms [published online ahead of print 27 July 2016], J Clin Pathol
  31. Oh, 2010, Novel mutations in the inhibitory adaptor protein LNK drive JAK-STAT signaling in patients with myeloproliferative neoplasms, Blood, 116, 988, 10.1182/blood-2010-02-270108 · DOI
  32. Rumi, 2016, LNK mutations in familial myeloproliferative neoplasms, Blood, 128, 144, 10.1182/blood-2016-04-711150 · DOI
  33. Lasho, 2010, LNK mutations in JAK2 mutation-negative erythrocytosis, N Engl J Med, 363, 1189, 10.1056/NEJMc1006966 · DOI
  34. Pardanani, 2010, LNK mutation studies in blast-phase myeloproliferative neoplasms, and in chronic-phase disease with TET2, IDH, JAK2 or MPL mutations, Leukemia, 24, 1713, 10.1038/leu.2010.163 · DOI
  35. Vainchenker, 2013, JAK/STAT signaling in hematological malignancies, Oncogene, 32, 2601, 10.1038/onc.2012.347 · DOI · Paper page
  36. Bandaranayake, 2012, Crystal structures of the JAK2 pseudokinase domain and the pathogenic mutant V617F, Nat Struct Mol Biol, 19, 754, 10.1038/nsmb.2348 · DOI
  37. Shan, 2014, Molecular basis for pseudokinase-dependent autoinhibition of JAK2 tyrosine kinase, Nat Struct Mol Biol, 21, 579, 10.1038/nsmb.2849 · DOI
  38. Leroy, 2016, Uncoupling JAK2 V617F activation from cytokine-induced signalling by modulation of JH2 αC helix, Biochem J, 473, 1579, 10.1042/BCJ20160085 · DOI
  39. Lu, 2005, Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation, Proc Natl Acad Sci USA, 102, 18962, 10.1073/pnas.0509714102 · DOI
  40. Ugo, 2004, Multiple signaling pathways are involved in erythropoietin-independent differentiation of erythroid progenitors in polycythemia vera, Exp Hematol, 32, 179, 10.1016/j.exphem.2003.11.003 · DOI
  41. Dawson, 2009, JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatin, Nature, 461, 819, 10.1038/nature08448 · DOI
  42. Liu, 2011, JAK2V617F-mediated phosphorylation of PRMT5 downregulates its methyltransferase activity and promotes myeloproliferation, Cancer Cell, 19, 283, 10.1016/j.ccr.2010.12.020 · DOI
  43. Staerk, 2006, An amphipathic motif at the transmembrane-cytoplasmic junction prevents autonomous activation of the thrombopoietin receptor, Blood, 107, 1864, 10.1182/blood-2005-06-2600 · DOI
  44. Balligand, 2016, Pathologic activation of thrombopoietin receptor and JAK2-STAT5 pathway by frameshift mutants of mouse calreticulin, Leukemia, 30, 1775, 10.1038/leu.2016.47 · DOI
  45. Chachoua, 2016, Thrombopoietin receptor activation by myeloproliferative neoplasm associated calreticulin mutants, Blood, 127, 1325, 10.1182/blood-2015-11-681932 · DOI
  46. Elf, 2016, Mutant calreticulin requires both its mutant C-terminus and the thrombopoietin receptor for oncogenic transformation, Cancer Discov, 6, 368, 10.1158/2159-8290.CD-15-1434 · DOI · Paper page
  47. Marty, 2016, Calreticulin mutants in mice induce an MPL-dependent thrombocytosis with frequent progression to myelofibrosis, Blood, 127, 1317, 10.1182/blood-2015-11-679571 · DOI
  48. Nivarthi, 2016, Thrombopoietin receptor is required for the oncogenic function of CALR mutants, Leukemia, 30, 1759, 10.1038/leu.2016.32 · DOI
  49. Araki, 2016, Activation of the thrombopoietin receptor by mutant calreticulin in CALR-mutant myeloproliferative neoplasms, Blood, 127, 1307, 10.1182/blood-2015-09-671172 · DOI
  50. Garbati, 2016, Mutant calreticulin-expressing cells induce monocyte hyperreactivity through a paracrine mechanism, Am J Hematol, 91, 211, 10.1002/ajh.24245 · DOI
  51. Mullally, 2010, Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells, Cancer Cell, 17, 584, 10.1016/j.ccr.2010.05.015 · DOI
  52. Hasan, 2013, JAK2V617F expression in mice amplifies early hematopoietic cells and gives them a competitive advantage that is hampered by IFNα, Blood, 122, 1464, 10.1182/blood-2013-04-498956 · DOI
  53. Tiedt, 2008, Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice, Blood, 111, 3931, 10.1182/blood-2007-08-107748 · DOI
  54. Li, 2010, JAK2 V617F impairs hematopoietic stem cell function in a conditional knock-in mouse model of JAK2 V617F-positive essential thrombocythemia, Blood, 116, 1528, 10.1182/blood-2009-12-259747 · DOI
  55. Grisouard, 2016, JAK2 exon 12 mutant mice display isolated erythrocytosis and changes in iron metabolism favoring increased erythropoiesis, Blood, 128, 839, 10.1182/blood-2015-12-689216 · DOI
  56. Balligand, 2016, Crispr/Cas9 engineered 61bp deletion in the Calr gene of mice leads to development of thrombocytosis [abstract], Blood, 128, 10.1182/blood.V128.22.4274.4274 · DOI
  57. Sangkhae, 2014, The thrombopoietin receptor, MPL, is critical for development of a JAK2V617F-induced myeloproliferative neoplasm, Blood, 124, 3956, 10.1182/blood-2014-07-587238 · DOI
  58. Walz, 2012, Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in mice, Blood, 119, 3550, 10.1182/blood-2011-12-397554 · DOI
  59. Grisouard, 2015, Deletion of Stat3 in hematopoietic cells enhances thrombocytosis and shortens survival in a JAK2-V617F mouse model of MPN, Blood, 125, 2131, 10.1182/blood-2014-08-594572 · DOI
  60. Pasquier, 2014, Myeloproliferative neoplasms: JAK2 signaling pathway as a central target for therapy, Clin Lymphoma Myeloma Leuk, 14, S23, 10.1016/j.clml.2014.06.014 · DOI
  61. Rampal, 2014, Genomic and functional analysis of leukemic transformation of myeloproliferative neoplasms, Proc Natl Acad Sci USA, 111, E5401, 10.1073/pnas.1407792111 · DOI · Paper page
  62. Stegelmann, 2010, High-resolution single-nucleotide polymorphism array-profiling in myeloproliferative neoplasms identifies novel genomic aberrations, Haematologica, 95, 666, 10.3324/haematol.2009.013623 · DOI
  63. Vannucchi, 2013, Mutations and prognosis in primary myelofibrosis, Leukemia, 27, 1861, 10.1038/leu.2013.119 · DOI
  64. Zhang, 2016, DNMT3A and TET2 compete and cooperate to repress lineage-specific transcription factors in hematopoietic stem cells, Nat Genet, 48, 1014, 10.1038/ng.3610 · DOI · Paper page
  65. Carbuccia, 2009, Mutations of ASXL1 gene in myeloproliferative neoplasms, Leukemia, 23, 2183, 10.1038/leu.2009.141 · DOI
  66. Kosmider, 2009, TET2 gene mutation is a frequent and adverse event in chronic myelomonocytic leukemia, Haematologica, 94, 1676, 10.3324/haematol.2009.011205 · DOI
  67. Ortmann, 2015, Effect of mutation order on myeloproliferative neoplasms, N Engl J Med, 372, 601, 10.1056/NEJMoa1412098 · DOI · Paper page
  68. Lundberg, 2014, Clonal evolution and clinical correlates of somatic mutations in myeloproliferative neoplasms, Blood, 123, 2220, 10.1182/blood-2013-11-537167 · DOI
  69. Stegelmann, 2011, DNMT3A mutations in myeloproliferative neoplasms, Leukemia, 25, 1217, 10.1038/leu.2011.77 · DOI · Paper page
  70. Challen, 2011, Dnmt3a is essential for hematopoietic stem cell differentiation, Nat Genet, 44, 23, 10.1038/ng.1009 · DOI · Paper page
  71. Quivoron, 2011, TET2 inactivation results in pleiotropic hematopoietic abnormalities in mouse and is a recurrent event during human lymphomagenesis, Cancer Cell, 20, 25, 10.1016/j.ccr.2011.06.003 · DOI · Paper page
  72. Xie, 2014, Age-related mutations associated with clonal hematopoietic expansion and malignancies, Nat Med, 20, 1472, 10.1038/nm.3733 · DOI · Paper page
  73. Chen, 2015, Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms, Blood, 125, 327, 10.1182/blood-2014-04-567024 · DOI
  74. Kameda, 2015, Loss of TET2 has dual roles in murine myeloproliferative neoplasms: disease sustainer and disease accelerator, Blood, 125, 304, 10.1182/blood-2014-04-555508 · DOI
  75. Guglielmelli, 2011, EZH2 mutational status predicts poor survival in myelofibrosis, Blood, 118, 5227, 10.1182/blood-2011-06-363424 · DOI
  76. Yang, 2016, Loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in a mouse model of myeloproliferative neoplasm, Blood, 127, 3410, 10.1182/blood-2015-11-679431 · DOI
  77. Shimizu, 2016, Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis, J Exp Med, 213, 1479, 10.1084/jem.20151136 · DOI
  78. Sashida, 2016, The loss of Ezh2 drives the pathogenesis of myelofibrosis and sensitizes tumor-initiating cells to bromodomain inhibition, J Exp Med, 213, 1459, 10.1084/jem.20151121 · DOI
  79. Abdel-Wahab, 2012, ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression, Cancer Cell, 22, 180, 10.1016/j.ccr.2012.06.032 · DOI
  80. Dey, 2012, Loss of the tumor suppressor BAP1 causes myeloid transformation, Science, 337, 1541, 10.1126/science.1221711 · DOI
  81. Hoischen, 2011, De novo nonsense mutations in ASXL1 cause Bohring-Opitz syndrome, Nat Genet, 43, 729, 10.1038/ng.868 · DOI
  82. Gelsi-Boyer, 2009, Mutations of polycomb-associated gene ASXL1 in myelodysplastic syndromes and chronic myelomonocytic leukaemia, Br J Haematol, 145, 788, 10.1111/j.1365-2141.2009.07697.x · DOI
  83. Abdel-Wahab, 2013, Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo, J Exp Med, 210, 2641, 10.1084/jem.20131141 · DOI
  84. Zhang, 2012, Genetic analysis of patients with leukemic transformation of myeloproliferative neoplasms shows recurrent SRSF2 mutations that are associated with adverse outcome, Blood, 119, 4480, 10.1182/blood-2011-11-390252 · DOI
  85. Wassie, 2015, A compendium of cytogenetic abnormalities in myelofibrosis: molecular and phenotypic correlates in 826 patients, Br J Haematol, 169, 71, 10.1111/bjh.13260 · DOI
  86. Komeno, 2015, SRSF2 is essential for hematopoiesis, and its myelodysplastic syndrome-related mutations dysregulate alternative pre-mRNA splicing, Mol Cell Biol, 35, 3071, 10.1128/MCB.00202-15 · DOI
  87. Harutyunyan, 2011, p53 lesions in leukemic transformation, N Engl J Med, 364, 488, 10.1056/NEJMc1012718 · DOI
  88. Courtier, Genomic analysis of myeloproliferative neoplasms in chronic and acute phases [published online ahead of print 14 October 2016], Haematologica
  89. Milosevic, 2012, Clinical significance of genetic aberrations in secondary acute myeloid leukemia, Am J Hematol, 87, 1010, 10.1002/ajh.23309 · DOI
  90. Tefferi, 2005, Pathogenesis of myelofibrosis with myeloid metaplasia, J Clin Oncol, 23, 8520, 10.1200/JCO.2004.00.9316 · DOI
  91. Plo, 2014, p53 at the crossroads of MPN treatment, Blood, 124, 668, 10.1182/blood-2014-06-579623 · DOI
  92. Arranz, 2014, Neuropathy of haematopoietic stem cell niche is essential for myeloproliferative neoplasms, Nature, 512, 78, 10.1038/nature13383 · DOI · Paper page
  93. Fleischman, 2011, TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms, Blood, 118, 6392, 10.1182/blood-2011-04-348144 · DOI
  94. Mager, 2015, IL-33 signaling contributes to the pathogenesis of myeloproliferative neoplasms, J Clin Invest, 125, 2579, 10.1172/JCI77347 · DOI
  95. Tapper, 2015, Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms, Nat Commun, 6, 6691, 10.1038/ncomms7691 · DOI
  96. Harutyunyan, 2016, Germline RBBP6 mutations in familial myeloproliferative neoplasms, Blood, 127, 362, 10.1182/blood-2015-09-668673 · DOI
  97. Saliba, 2015, Germline duplication of ATG2B and GSKIP predisposes to familial myeloid malignancies, Nat Genet, 47, 1131, 10.1038/ng.3380 · DOI
  98. Grand, 2009, Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms, Blood, 113, 6182, 10.1182/blood-2008-12-194548 · DOI
  99. Tefferi, 2010, IDH1 and IDH2 mutation studies in 1473 patients with chronic-, fibrotic- or blast-phase essential thrombocythemia, polycythemia vera or myelofibrosis, Leukemia, 24, 1302, 10.1038/leu.2010.113 · DOI
  100. Klampfl, 2011, Genome integrity of myeloproliferative neoplasms in chronic phase and during disease progression, Blood, 118, 167, 10.1182/blood-2011-01-331678 · DOI
  101. Lasho, 2012, SF3B1 mutations in primary myelofibrosis: clinical, histopathology and genetic correlates among 155 patients, Leukemia, 26, 1135, 10.1038/leu.2011.320 · DOI
  102. Lacout, 2006, JAK2V617F expression in murine hematopoietic cells leads to MPD mimicking human PV with secondary myelofibrosis, Blood, 108, 1652, 10.1182/blood-2006-02-002030 · DOI
  103. Wernig, 2006, Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model, Blood, 107, 4274, 10.1182/blood-2005-12-4824 · DOI
  104. Zaleskas, 2006, Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617F, PLoS One, 1, e18, 10.1371/journal.pone.0000018 · DOI
  105. Xing, 2008, Transgenic expression of JAK2V617F causes myeloproliferative disorders in mice, Blood, 111, 5109, 10.1182/blood-2007-05-091579 · DOI
  106. Shide, 2008, Development of ET, primary myelofibrosis and PV in mice expressing JAK2 V617F, Leukemia, 22, 87, 10.1038/sj.leu.2405043 · DOI
  107. Etheridge, 2014, JAK2V617F-positive endothelial cells contribute to clotting abnormalities in myeloproliferative neoplasms, Proc Natl Acad Sci USA, 111, 2295, 10.1073/pnas.1312148111 · DOI
  108. Zhan, 2016, JAK2(V617F)-mutant megakaryocytes contribute to hematopoietic stem/progenitor cell expansion in a model of murine myeloproliferation, Leukemia, 30, 2332, 10.1038/leu.2016.114 · DOI
  109. Marty, 2010, Myeloproliferative neoplasm induced by constitutive expression of JAK2V617F in knock-in mice, Blood, 116, 783, 10.1182/blood-2009-12-257063 · DOI
  110. Li, 2014, JAK2V617F homozygosity drives a phenotypic switch in myeloproliferative neoplasms, but is insufficient to sustain disease, Blood, 123, 3139, 10.1182/blood-2013-06-510222 · DOI
  111. Akada, 2010, Conditional expression of heterozygous or homozygous Jak2V617F from its endogenous promoter induces a polycythemia vera-like disease, Blood, 115, 3589, 10.1182/blood-2009-04-215848 · DOI
  112. Akada, 2012, Erythroid lineage-restricted expression of Jak2V617F is sufficient to induce a myeloproliferative disease in mice, Haematologica, 97, 1389, 10.3324/haematol.2011.059113 · DOI
  113. Lamrani, 2014, Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm, Blood, 124, 1136, 10.1182/blood-2013-10-530832 · DOI
  114. Shide, Calreticulin mutant mice develop essential thrombocythemia that is ameliorated by the JAK inhibitor ruxolitinib [published online ahead of print 29 November 2016]

Cited by

See all 616

Metadata

Authors
Vainchenker, W., & Kralovics, R.
Venue
Blood
Publisher
American Society of Hematology
Published
2017-02-09
Volume
129
Issue
6
Pages
667-679
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2016-10-695940
Cited by
616
References
12
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review