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Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?

Hasselbalch, Hans Carl·2012·Blood
DOI 10.1182/blood-2011-11-394775
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Abstract

The morbidity and mortality of patients with the chronic Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primary myelofibrosis are mainly caused by cardiovascular diseases, thrombohemorrhagic complications, and bone marrow failure because of myelofibrosis and leukemic transformation. In the general population, chronic inflammation is considered of major importance for the development of atherosclerosis and cancer. MPNs are characterized by a state of chronic inflammation, which is proposed to be the common denominator for the development of “premature atherosclerosis,” clonal evolution, and second cancer in patients with MPNs. Chronic inflammation may both initiate clonal evolution and catalyze its expansion from early disease stage to the myelofibrotic burnt-out phase. Furthermore, chronic inflammation may also add to the severity of cardiovascular disease burden by accelerating the development of atherosclerosis, which is well described and recognized in other chronic inflammatory diseases. A link between chronic inflammation, atherosclerosis, and second cancer in MPNs favors early intervention at the time of diagnosis (statins and interferon-α2), the aims being to dampen chronic inflammation and clonal evolution and thereby also diminish concurrent disease-mediated chronic inflammation and its consequences (accelerated atherosclerosis and second cancer).

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Research works printed but not linked: 90

  1. Campbell, 2006, Mechanisms of disease: the myeloproliferative disorders., N Engl J Med, 355, 2452, 10.1056/NEJMra063728 · DOI
  2. Tefferi, 2010, Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH, IKZF1., Leukemia, 24, 1128, 10.1038/leu.2010.69 · DOI
  3. Barbui, 2011, Inflammation and thrombosis in essential thrombocythemia and polycythemia vera: different role of C-reactive protein and pentraxin 3., Haematologica, 96, 315, 10.3324/haematol.2010.031070 · DOI
  4. Hasselbalch, 1990, Idiopathic myelofibrosis: a clinical study of 80 patients., Am J Hematol, 34, 291, 10.1002/ajh.2830340411 · DOI
  5. Kristinsson, 2010, Autoimmunity and the risk of myeloproliferative neoplasms., Haematologica, 95, 1216, 10.3324/haematol.2009.020412 · DOI
  6. Hansson, 2011, The immune system in atherosclerosis., Nat Immunol, 12, 204, 10.1038/ni.2001 · DOI
  7. Sherer, 2006, Mechanisms of disease: atherosclerosis in autoimmune diseases., Nat Clin Pract Rheumatol, 2, 99, 10.1038/ncprheum0092 · DOI
  8. Rho, 2009, Inflammatory mediators and premature coronary atherosclerosis in rheumatoid arthritis., Arthritis Rheum, 61, 1580, 10.1002/art.25009 · DOI
  9. Alexandroff, 2009, More than skin deep: atherosclerosis as a systemic manifestation of psoriasis., Br J Dermatol, 161, 1, 10.1111/j.1365-2133.2009.09281.x · DOI
  10. Hahn, 2003, Systemic lupus erythematosus and accelerated atherosclerosis., N Engl J Med, 349, 2379, 10.1056/NEJMp038168 · DOI
  11. Goldberg, 2009, Cytokine and cytokine-like inflammation markers, endothelial dysfunction, and imbalanced coagulation in development of diabetes and its complications., J Clin Endocrinol Metab, 94, 3171, 10.1210/jc.2008-2534 · DOI
  12. Prandoni, 2003, An association between atherosclerosis and venous thrombosis., N Engl J Med, 348, 1435, 10.1056/NEJMoa022157 · DOI
  13. Bisoendial, 2007, C-reactive protein and atherogenesis: from fatty streak to clinical event., Atherosclerosis, 195, e10, 10.1016/j.atherosclerosis.2007.04.053 · DOI
  14. Verma, 2006, Is C-reactive protein an innocent bystander or proatherogenic culprit? C-reactive protein promotes atherothrombosis., Circulation, 113, 2135
  15. Emerging Risk Factors Collaboration, 2010, C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis., Lancet, 375, 132, 10.1016/S0140-6736(09)61717-7 · DOI · Paper page
  16. Totani, 2010, Platelet-leukocyte interactions in cardiovascular disease and beyond., Arterioscler Thromb Vasc Biol, 30, 2357, 10.1161/ATVBAHA.110.207480 · DOI
  17. Lindahl, 2000, Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease., N Engl J Med, 343, 1139, 10.1056/NEJM200010193431602 · DOI
  18. Peri, 2000, PTX3, a prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans., Circulation, 102, 636, 10.1161/01.CIR.102.6.636 · DOI
  19. Elliott, 2005, Thrombosis and haemorrhage in polycythaemia vera and essential thrombocythaemia., Br J Haematol, 128, 275, 10.1111/j.1365-2141.2004.05277.x · DOI
  20. Landolfi, 2011, Pathophysiology of thrombosis in myeloproliferative neoplasms., Haematologica, 96, 183, 10.3324/haematol.2010.038299 · DOI
  21. Di Nisio, 2007, The haematocrit and platelet target in polycythemia vera., Br J Haematol, 136, 249, 10.1111/j.1365-2141.2006.06430.x · DOI
  22. Falanga, 2007, V617F JAK-2 mutation in patients with essential thrombocythemia: relation to platelet, granulocyte, and plasma hemostatic and inflammatory molecules., Exp Hematol, 35, 702, 10.1016/j.exphem.2007.01.053 · DOI
  23. Barbui, 2009, Perspectives on thrombosis in essential thrombocythemia and polycythemia vera: is leukocytosis a causative factor?, Blood, 114, 759, 10.1182/blood-2009-02-206797 · DOI
  24. Carobbio, 2011, Risk factors for arterial and venous thrombosis in WHO-defined essential thrombocythemia: an international study of 891 patients., Blood, 117, 5857, 10.1182/blood-2011-02-339002 · DOI
  25. Quist-Paulsen, 2010, Arterial cardiovascular risk factors and venous thrombosis: results from a population-based, prospective study (the HUNT 2)., Haematologica, 95, 119, 10.3324/haematol.2009.011866 · DOI
  26. Norata, 2009, Deficiency of the long pentraxin PTX3 promotes vascular inflammation and atherosclerosis., Circulation, 120, 699, 10.1161/CIRCULATIONAHA.108.806547 · DOI
  27. Pamuk, 2006, Role of insulin resistance in increased frequency of atherosclerosis detected by carotid ultrasonography in rheumatoid arthritis., J Rheumatol, 33, 2447
  28. La Montagna, 2007, Insulin resistance is an independent risk factor for atherosclerosis in rheumatoid arthritis., Diab Vasc Dis Res, 4, 130, 10.3132/dvdr.2007.031 · DOI
  29. Kato, 2005, Status of endothelial dependent vasodilation in patients with hyperuricemia., Am J Cardiol, 96, 1576, 10.1016/j.amjcard.2005.07.068 · DOI
  30. Tomiyama, 2011, Relationships among hyperuricemia, metabolic syndrome, and endothelial function., Am J Hypertens, 24, 770, 10.1038/ajh.2011.55 · DOI
  31. Goicoechea, 2010, Effect of allopurinol in chronic kidney disease progression and cardiovascular risk., Clin J Am Soc Nephrol, 5, 1388, 10.2215/CJN.01580210 · DOI
  32. Said, 2011, Myeloproliferative neoplasms cause glomerulopathy., Kidney Int, 80, 753, 10.1038/ki.2011.147 · DOI
  33. Hussain, 2007, Inflammation and cancer: an ancient link with novel potentials., Int J Cancer, 121, 2373, 10.1002/ijc.23173 · DOI
  34. Mantovani, 2010, Molecular pathways and targets in cancer-related inflammation., Ann Med, 42, 161, 10.3109/07853890903405753 · DOI
  35. Balkwill, 2001, Inflammation and cancer: back to Virchow?, Lancet, 357, 539, 10.1016/S0140-6736(00)04046-0 · DOI · Paper page
  36. Karin, 2005, NF-kappaB: linking inflammation and immunity to cancer development and progression., Nat Rev Immunol, 5, 749, 10.1038/nri1703 · DOI
  37. Martin, 2009, Autoimmunity and hematologic malignancies: associations and mechanisms., Leuk Lymphoma, 50, 541, 10.1080/10428190902780677 · DOI
  38. Smedby, 2008, Autoimmune and inflammatory disorders and risk of malignant lymphomas: an update., J Intern Med, 264, 514, 10.1111/j.1365-2796.2008.02029.x · DOI
  39. van de Schans, 2011, Excess of autoimmune and chronic inflammatory disorders in patients with lymphoma compared with all cancer patients: a cancer registry-based analysis in the south of the Netherlands., Autoimmun Rev, 10, 228, 10.1016/j.autrev.2010.11.001 · DOI
  40. Kristinsson, 2011, Chronic immune stimulation might act as a trigger for the development of acute myeloid leukemia or myelodysplastic syndromes., J Clin Oncol, 29, 2897, 10.1200/JCO.2011.34.8540 · DOI · Paper page
  41. Panteli, 2005, Serum interleukin (IL)-1, IL-2, sIL-2Ra, IL-6 and thrombopoietin levels in patients with chronic myeloproliferative diseases., Br J Haematol, 130, 709, 10.1111/j.1365-2141.2005.05674.x · DOI
  42. Tefferi, 2011, Circulating interleukin (IL)-8, IL-2R, IL-12, and IL-15 levels are independently prognostic in primary myelofibrosis: a comprehensive cytokine profiling study., J Clin Oncol, 29, 1356, 10.1200/JCO.2010.32.9490 · DOI
  43. Skov, 2011, Whole blood transcriptional profiling of interferon-inducible genes identifies highly upregulated IFI27 in primary myelofibrosis., Eur J Haematol, 87, 54, 10.1111/j.1600-0609.2011.01618.x · DOI
  44. Skov, 2010, Gene expression profiling with principal component analysis depicts the biological continuum from essential thrombocythemia over polycythemia vera to myelofibrosis [abstract]., Blood (ASH Annual Meeting Abstracts), 116, 4115
  45. Vannucchi, 2009, Increased risk of lymphoid neoplasms in patients with Philadelphia chromosome-negative myeloproliferative neoplasms., Cancer Epidemiol Biomarkers Prev, 18, 2068, 10.1158/1055-9965.EPI-09-0353 · DOI
  46. Frederiksen, 2011, Chronic myeloproliferative neoplasms and subsequent cancer risk: a Danish population-based cohort study., Blood, 118, 6515, 10.1182/blood-2011-04-348755 · DOI
  47. Voulgarelis, 2004, Myelodysplasia-associated autoimmunity: clinical and pathophysiologic concepts., Eur J Clin Invest, 34, 690, 10.1111/j.1365-2362.2004.01417.x · DOI
  48. Rondeau, 1983, Immune disorders in agnogenic myeloid metaplasia: relations to myelofibrosis., Br J Haematol, 53, 467, 10.1111/j.1365-2141.1983.tb02048.x · DOI
  49. Hasselbalch, 1985, Circulating immune complexes in myelofibrosis., Scand J Haematol, 34, 177, 10.1111/j.1600-0609.1985.tb02252.x · DOI
  50. Rizzi, 2004, Autoimmune myelofibrosis: report of three cases and review of the literature., Leuk Lymphoma, 45, 561, 10.1080/10428190310001597982 · DOI
  51. Barosi, 2010, Does auto-immunity contribute to anemia in myeloproliferative neoplasms (MPN)-associated myelofibrosis?, Leuk Res, 34, 1119, 10.1016/j.leukres.2010.05.010 · DOI
  52. Hermouet, 2011, The JAK2 46/1 haplotype: a marker of inappropriate myelomonocytic response to cytokine stimulation, leading to increased risk of inflammation, myeloid neoplasm, and impaired defence against infection?, Haematologica, 96, 1575, 10.3324/haematol.2011.055392 · DOI
  53. Nielsen, 2011, The JAK2 V617F somatic mutation, mortality and cancer risk in the general population., Haematologica, 96, 450, 10.3324/haematol.2010.033191 · DOI
  54. Dong, 2006, Role of transforming growth factor-beta in hematologic malignancies., Blood, 107, 4589, 10.1182/blood-2005-10-4169 · DOI
  55. Johnson, 2007, Vascular endothelial growth factor and immunosuppression in cancer: current knowledge and potential for new therapy., Expert Opin Biol Ther, 7, 449, 10.1517/14712598.7.4.449 · DOI
  56. Fleischman, 2011, Tumor necrosis factor-alpha facilitates clonal expansion of JAK2V617F-positive cells in myeloproliferative neoplasms., Blood, 118, 6392, 10.1182/blood-2011-04-348144 · DOI
  57. Barrett, 2008, Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease., Nat Genet, 40, 955, 10.1038/ng.175 · DOI · Paper page
  58. Ferguson, 2010, Genetic factors in chronic inflammation: single nucleotide polymorphisms in the STAT-JAK pathway, susceptibility to DNA damage and Crohn's disease in a New Zealand population., Mutat Res, 690, 108, 10.1016/j.mrfmmm.2010.01.017 · DOI
  59. Pardanani, 2008, Host genetic variation contributes to phenotypic diversity in myeloproliferative disorders., Blood, 111, 2785, 10.1182/blood-2007-06-095703 · DOI
  60. Kilpivaara, 2009, A germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive myeloproliferative neoplasms., Nat Genet, 41, 455, 10.1038/ng.342 · DOI
  61. Jones, 2009, JAK2 haplotype is a major risk factor for the development of myeloproliferative neoplasms., Nat Genet, 41, 446, 10.1038/ng.334 · DOI
  62. Olcaydu, 2009, A common JAK2 haplotype confers susceptibility to myeloproliferative neoplasms., Nat Genet, 41, 450, 10.1038/ng.341 · DOI
  63. Tefferi, 2010, JAK2 germline genetic variation affects disease susceptibility in primary myelofibrosis regardless of V617F mutational status: nullizygosity for the JAK2 46/1 haplotype is associated with inferior survival., Leukemia, 24, 105, 10.1038/leu.2009.225 · DOI
  64. Jones, 2010, The JAK2 46/1 haplotype predisposes to MPL-mutated myeloproliferative neoplasms., Blood, 115, 4517, 10.1182/blood-2009-08-236448 · DOI
  65. Plo, 2008, JAK2 stimulates homologous recombination and genetic instability: potential implication in the heterogeneity of myeloproliferative disorders., Blood, 112, 1402, 10.1182/blood-2008-01-134114 · DOI
  66. Hanahan, 2000, The hallmarks of cancer., Cell, 100, 57, 10.1016/S0092-8674(00)81683-9 · DOI · Paper page
  67. Beg, 1996, An essential role for NF-kappaB in preventing TNF-alpha induced cell death., Science, 274, 782, 10.1126/science.274.5288.782 · DOI · Paper page
  68. Pikarsky, 2004, NF-kappaB functions as a tumour promoter in inflammation-associated cancer., Nature, 431, 461, 10.1038/nature02924 · DOI
  69. Balkwill, 2002, Tumor necrosis factor or tumor promoting factor?, Cytokine Growth Factor Rev, 13, 135, 10.1016/S1359-6101(01)00020-X · DOI · Paper page
  70. Pittet, 2011, Monocytes link atherosclerosis and cancer., Eur J Immunol, 41, 2519, 10.1002/eji.201141727 · DOI
  71. Elliott, 2007, Monocytosis is an adverse prognostic factor for survival in younger patients with primary myelofibrosis., Leuk Res, 31, 1503, 10.1016/j.leukres.2006.12.025 · DOI
  72. Qian, 2010, Macrophage diversity enhances tumor progression and metastasis., Cell, 141, 39, 10.1016/j.cell.2010.03.014 · DOI
  73. Mantovani, 2011, Cancer-promoting tumor-associated macrophages: new vistas and open questions., Eur J Immunol, 41, 2522, 10.1002/eji.201141894 · DOI
  74. Marchioli, 2005, Vascular and neoplastic risk in a large cohort of patients with polycythemia vera., J Clin Oncol, 23, 2224, 10.1200/JCO.2005.07.062 · DOI
  75. Monaco, 2004, Canonical pathway of nuclear factor kappa B activation selectively regulates proinflammatory and prothrombotic responses in human atherosclerosis., Proc Natl Acad Sci U S A, 101, 5634, 10.1073/pnas.0401060101 · DOI
  76. Venuraju, 2010, Osteoprotegerin as a predictor of coronary artery disease and cardiovascular mortality and morbidity., J Am Coll Cardiol, 55, 2049, 10.1016/j.jacc.2010.03.013 · DOI
  77. Lieb, 2010, Biomarkers of the osteoprotegerin pathway: clinical correlates, subclinical disease, incident cardiovascular diseases and mortality., Arterioscler Thromb Vasc Biol, 30, 1849, 10.1161/ATVBAHA.109.199661 · DOI
  78. Rameshwar, 1994, Monocyte adhesion in patients with bone marrow fibrosis is required for the production of fibrogenic cytokines: potential role for interleukin-1 and TGF-beta., J Immunol, 153, 2819, 10.4049/jimmunol.153.6.2819 · DOI
  79. Rameshwar, 1998, Systemic transforming growth factor-beta in patients with bone marrow fibrosis: pathophysiological implications., Am J Hematol, 59, 133, 10.1002/(SICI)1096-8652(199810)59:2<133::AID-AJH6>3.0.CO;2-Z · DOI
  80. Komura, 2005, Role for the nuclear factor kappaB pathway in transforming growth factor-beta1 production in idiopathic myelofibrosis: possible relationship with FK506 binding protein 51 overexpression., Cancer Res, 65, 3281, 10.1158/0008-5472.CAN-04-2339 · DOI
  81. Oku, 2010, JAK2 V617F uses distinct signalling pathways to induce cell proliferation and neutrophil activation., Br J Haematol, 150, 334, 10.1111/j.1365-2141.2010.08249.x · DOI · Paper page
  82. Coller, 2005, Leukocytosis and ischemic vascular disease morbidity and mortality: is it time to intervene?, Arterioscler Thromb Vasc Biol, 25, 658, 10.1161/01.ATV.0000156877.94472.a5 · DOI · Paper page
  83. 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
  84. Verstovsek, 2010, A. Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis., N Engl J Med, 363, 1117, 10.1056/NEJMoa1002028 · DOI
  85. Rambaldi, 2010, A pilot study of the histone-deacetylase inhibitor givinostat in patients with JAK2V617F positive chronic myeloproliferative neoplasms., Br J Haematol, 150, 446, 10.1111/j.1365-2141.2010.08266.x · DOI
  86. Andersen, 2011, A Phase II study of vorinostat (MK-0683) in patients with polycythaemia vera essential thrombocythaemia [abstract].
  87. Hasselbalch, 2006, Statins in the treatment of polycythaemia vera and allied disorders: an antithrombotic and cytoreductive potential?, Leuk Res, 30, 1217, 10.1016/j.leukres.2005.12.018 · DOI
  88. Griner, 2011, A mechanistic rationale for the use of statins to enhance JAK2 inhibitor therapy in MPNs [abstract]., Blood (ASH Annual Meeting Abstracts), 118
  89. Hasselbalch, 2009, Myelofibrosis with myeloid metaplasia: the advanced phase of an untreated disseminated hematological cancer: time to change our therapeutic attitude with early upfront treatment?, Leuk Res, 33, 11, 10.1016/j.leukres.2008.06.002 · DOI
  90. Hasselbalch, 2011, A new era for interferon-alpha2 in the treatment of Philadelphia-negative chronic myeloproliferative neoplasms., Expert Rev Hematol, 4, 637, 10.1586/ehm.11.63 · DOI

Cited by

Metadata

Authors
Hasselbalch, H. C.
Venue
Blood
Publisher
American Society of Hematology
Published
2012-04-05
Volume
119
Issue
14
Pages
3219-3225
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2011-11-394775
Cited by
300
References
10
Language
en

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