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92(9):1266-7. 36. Bensinger TA, Gillette PN. Hemolysis in sickle cell disease. Arch Intern Med. 1974;133:624-31. 37. Gladwin MT, Sachdev V, Jison ML, et al. Pulmonary hypertension as a risk factor for death in patients with sickle cell disease. N Engl J Med. 2004;350:886-95. 38. Kato GJ, McGowan V, Machado RF, et al. Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease. Blood. 2006;107: 2279-85. 39. Bunn HF, Nathan DG, Dover GJ, Hebbel RP, Platt OS, Rosse WF, Ware RE. Pulmonary hypertension and nitric oxide depletion in sickle cell disease. Blood. 2010;116(5):687-92. 40. Hebbel RP. Reconstructing sickle cell disease: a data-based analysis of the “hyper-hemolysis paradigm” for pulmonary hypertension from the perspective of evidence-based medicine. Am J Hematol., 2011;86(2):123-154. 41. Wagener FA, Eggert A, Boerman OC, et al. Heme is a potent inducer of inflammation in mice and is counteracted by heme oxygenase. Blood. 2001;98:1802-11. 42. Lee A, Thomas P, Cupidore L, Serjeant B, Serjeant G. Improved survival in homozygous sickle cell disease: lessons from a cohort study. Br Med J. 1995;311:1600-2. 43. Platt OS, Thorington BD, Brambilla DJ, et al. Pain in sickle cell disease. Rates and risk factors. N Engl J Med. 1991;325:11-6. 44. Platt OS, Brambilla DJ, Rosse WF, et al. Mortality in sickle cell disease: life expectancy and risk factors for early death. N Engl J Med. 1994;330:1639-44. 45. McClish DK, Smith WR, Dahman BA, et al. Pain site frequency and location in sickle cell disease. Pain. 2009;145(1-2):246-51. 46. Vichinsky EP, Neumayr LD, Earles AN, et al. Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group. N Engl J Med. 2000;342:1855-65. 47. Ohene-Frempong K, Weiner SJ, Sleeper LA, et al. Cerebrovascular accidents in sickle cell disease: rates and risk factors. Blood. 1998;91(1):288-94. 48. Smith WR, Bovbjerg VE, Penberthy LT, et al. Understanding pain and improving management of sickle cell disease: the PiSCES study. J Natl Med Assoc. 2005;97(2):183-93. 49. Miller ST, Sleeper LA, Pegelow CH, et al. Prediction of adverse outcomes in children with sickle cell disease. N Engl J Med. 2000; 342:83-9. 50. Frenette PS. Sickle cell vaso-occlusion: heterotypic, multicellular aggregations driven by leukocyte adhesion. Microcirculation. 2004;11(2):167-77. 51. Quinn CT, Rogers ZR, McCavit TL, Buchanan GR. Improved survival of children and adolescents with sickle cell disease. Blood. 2010;115:3447-52. 52. Sebastiani P, Solovieff N, Hartley SW, et al. Genetic modifiers of the severity of sickle cell anemia identified through a genomewide association study. Am J Hematol. 2010;85(1):29-35. 53. Van Beers EJ, van Tuijn CF, Nieuwkerk PT, Friederich PW, Vranken JH, Biemond BJ. Patient-controlled analgesia versus continous infusion of morphine during vaso-occlusive crisis in sickle cell disease, a randomized controlled trial. Am J Hematol. 2007;82(11):955-60. 54. Griffin TC, McIntire D, Buchanan GR. High-dose intravenous methylprednisolone therapy for pain in children and adolescents with sickle cell disease. N Engl J Med. 1994;330(11):773-7. 55. Strouse JJ, Takemoto CM, Keefer JR, Kato GJ, Casella JF. Corticosteroids and increased risk of readmission after acute chest syndrome in children with sickle cell disease. Pediatr Blood Cancer. 2008;50(5):1006-12. 56. Solanki DL. Sickle cell anemia, oxygen treatment, and anaemic crisis. Br Med J. 1983;287:725-6. 57. Lane PK, Embury SH, Toy PT. Oxygen induced marrow red cell hypoplasia leading to transfusion in sickle painful crisis. Am J Hematol. 1988;27:67-8. 58. Adams-Graves P, Kedar A, Koshy M, et al. RheothRx (poloxamer 188) injection for the acute painful episode of sickle cell disease: a pilot study. Blood. 1997;90(5):2041-6. 59. Ataga KI, Smith WR, DeCastro LM, et al. Efficacy and safety of the Gardos Channel blocker, senicapoc (ICA-17043), in patients with sickle cell anemia. Blood. 2008;111(8):3991-7. 60. Chang J, Shi PA, Chiang EY, Frenette PS. Intravenous immunoglobulins reverse acute vaso-occlusive crises in sickle cell mice through rapid inhibition of neutrophil adhesion. Blood. 2008;111(2):915-23. London, United Kingdom, June 9-12, 2011 61. Kaul DK, Tsai HM, Liu XD, et al. Monoclonal antibodies to alphaVbeta3 (7E3 and LM609) inhibit sickle red blood cellendothelium interactions induced by platelet-activating factor. Blood. 2000;95:368-74. 62. Finnegan EM, Barabino GA, Liu XS, Chang HY, Jonczyk A, Kaul DK. Small-molecule cyclic alpha V beta 3 antagonists inhibit sickle red cell adhesion to vascular endothelium and vasooclusion. Am J Physiol. 2007;293(2):H1038-45. 63. Chang J, Patton JT, Sarkar A, Ernst B, Magnani JL, Frenette PS. GMI-1070, a novel pan-selectin antagonist, reverses acute vascular occlusions in sickle cell mice. Blood. 2010;116(10):1779-86. 64. Solovey AA, Solovey AN, Harkness J, Hebbel RP. Modulation of endothelial cell activation in sickle cell disease: a pilot study. Blood. 2001;97(7):1937-41. 65. Head CA, Swerdlow P, McDade WA, et al. Beneficial effects of nitric oxide breathing in adult patients with sickle cell crisis. Am J Hematol. 2010;85(10):800-2. 66. Hebbel RP, Vercellotti GM, Pace BS, et al. The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular biology of sickle transgenic mice. Blood. 2010;115(12):2483-90. 67. Hebbel RP, Vercellotti G, Nath KA. A systems biology consideration of the vasculopathy of sickle cell anemia: the need for multi-modality chemo-prophylaxis. Curr Drug Targets Cardiovasc Haematol Disord. 2009;9(4):271-92. 68. Charache S, Dover GJ, Moore RD, et al. Hydroxyurea: effects on hemoglobin F production in patients with sickle cell anemia. Blood. 1992;79(10):2555-65. 69. Charache S, Terrin ML, Moore RD, et al. Effect of hydroxyurea on the frequency of painful crises in sickle cell anemia. Investigators of the Multicenter Study of Hydroxyurea in Sickle Cell Anemia. N Engl J Med. 1995; 332:1317-22. 70. Kinney TR, Helms RW, O’Branski EE, et al. Safety of hydroxyurea in children with sickle cell anemia: results of the HUG- KIDS study, a phase I/II Pediatric Hydroxyurea Group. Blood. 1999;94(5):1550-4. 71. Wang WC, Wynn LW, Rogers ZR, Scott JP, Lane PA, Ware RE. A two-year pilot trial of hydroxyurea in very young children with sickle-cell anemia. J Pediatr. 2001;139(6):790-6. 72. Ware RE. How I use hydroxyurea to treat young patients with sickle cell anemia. Blood. 2010;115(26):5300-11. 73. Hillery CA, Du MC, Wang WC, Scott JP. Hydroxyurea therapy decreases the in vitro adhesion of sickle erythrocytes to thrombospondin and laminin. Br J Haematol. 2000;109:322-7. 74. Gambero S, Canalli AA, Traina F, et al. Therapy with hydroxyurea is associated with reduced adhesion molecule gene and protein expression in sickle red cells with a concomitant reduction in adhesive properties. Eur J Haematol. 2007;78(2):144-51. 75. Cartron JP, Elion J. Erythroid adhesion molecules in sickle cell disease: effect of hydroxyurea. Trans Clin Biol. 2008;15(1-2):39-50. 76. Odievre MH, Bony V, Benkerrou M, et al. Modulation of erythroid adhesion receptor expression by hydroxyurea in children with sickle cell disease. Haematologica. 2008;93:502-10. 77. Styles LA, Lubin B, Vichinsky E, et al. Decrease of very late activation antigen-4 and CD36 on reticulocytes in sickle cell patients treated with hydroxyurea. Blood. 1997;89:2554-9. 78. Haynes J Jr, Obiako B, Hester RB, Baliga BS, Stevens T. Hydroxyurea attenuates activated neutrophil-mediated sickle erythrocyte membrance phosphatidylserine exposure and adhesion to pulmonary vascular endothelium. Am J Phys. 2008; 294(1):H379-85. 79. Laurance S, Pellay FX, Dossou-Yovo OP, et al. Hydroxycarbamide stimulates the production of proinflammatory cytokines by endothelial cells: relevance to sickle cell disease. Pharmacogenetics Genomics. 2010;20(4):257-68. 80. Lapoumeroulie C, Benkerrou M, Odievre MH, et al. Decreased plasma endothelin-1 levels in children with sickle cell disease treated with hydroxyurea. Haematologica. 2005;90:401-3. 81. Lanaro C, Franco-Penteado CF, Albuqueque DM, Saad ST, Conran N, Costa FF. Altered levels of cytokines and inflammatory mediators in plasma and leukocytes of sickle cell anemia patients and effects of hydroxyurea therapy. J Leuk Biol. 2009; 85(2):235-42. 82. McGann PT, Ware RE. Hydroxyurea for sickle cell anemia: what have we learned and what questions remain? Curr Opin Hematol., 2011;18(3):158-165. Hematology Education: the education programme for the annual congress of the European Hematology Association | 2011; 5(1) | 329 |
M. Boeckh Vaccine and Infectious Disease Division and Clinical Research Division, Fred Hutchinson Cancer Research Center, and Department of Medicine, University of Washington, Seattle, OR, USA Funding: This work was partially supported by NIH grants CA18029, CA15704, and HL93294. M.B. received research funding from Viropharma Inc., Chimerix Inc., Vical Inc., Roche Pharmaceuticals, Glaxo- Smith-Kline, and Adamas Pharmaceuticals, served as a consultant for Novartis, Astellas, Gilead, Chimerix Inc., Vical Inc., Boehringer Ingelheim, and Roche/Genentech. He served on DSMBs for Pfizer and for an influenza vaccine study funded byUS Government funds from the Office for Preparedness and Response, Biomedical Advanced Research and Development Authority, under contract to DynPort Vaccine Company. Hematology Education: the education program for the annual congress of the European Hematology Association 2011;5:330-336 Supportive care of transplants Treatment of viral infections after hematopoietic cell transplantation Introduction Viral infections are a major complication after hematopoietic cell transplantation (HCT). Patients are at risk for complications of viruses that reactivate from latency (e.g., herpes viruses), as well as those that are acquired exogenously (e.g., respiratory viruses). Major progress has been made in the management of cytomegalovirus, historically the most deadly of all viruses, but challenges remain with effective management of a large spectrum of viral disease. This review will summarize recent developments in the treatment of viral diseases. Prophylactic strategies are not reviewed here. The reader is also referred to published guidelines that have recently been endorsed by a wide range of international professional societies, 1-4 as well as recently published comprehensive reviews of management options for the most relevant viruses, including cytomegalo virus (CMV), Epstein– Barr Virus (EBV), influenza virus, adenovirus, and respiratory syncytial virus. 5-9 Due to a paucity of randomized trials, many treatment recommendations are based on expert opinion. Adenoviruses Adenovirus disease is an emerging problem in HCT recipients. Disease occurs mainly in patients with profoundly reduced T cell function (i.e., following in vivo or ex vivo T cell depletion) but sporadic cases in non-T cell depleted patients can occur. 10 The outcome is often fatal, especially in the presence of low lymphocyte counts. 10 Treatment options are very limited and consist presently of cidofovir and ribavirin. No randomized trial has been performed and neither drug is approved for this indication. Presently, cidofovir is considered the treatment of choice. 8 A B S T R A C T Viral infections are important complications after hematopoietic cell transplantation. Progress has been made in the management of cytomegalovirus and other herpes viruses, as well as influenza. However, for many viral diseases, there are either no or only moderately active treatment options available. This review will provide an overview of currently available treatment options and define areas of need for future development of therapeutics. (Table 1). Two dose regimens are available, that is, 5 mg/kg once a week or 1 mg/kg three times per week. 11,12 The latter may be less toxic but does not cover CMV. Ribavirin treatment has shown variable results, possibly due to strain-specific susceptibilities. We occasionally use a trial of ribavirin in addition to cidofovir or by itself in salvage situations with close viral load monitoring. Reduction of immunosuppression should be attempted given the strong correlation of lymphocyte recovery with outcome; 8 however, this is often not feasible. A newer compound (i.e., CMX-001, Chimerix Inc.) with potentially higher activity, and an improved toxicity profile is presently under investigation. 13,14 Treatment with donor-derived adenovirus-specific T cells is being studied at several centers. 8 Respiratory viruses Respiratory syncytial virus RSV RSV pneumonia carries a high mortality in highly immunosuppressed HCT recipients. However, recovery from RSV lower respiratory tract disease without specific treatment has also been reported. 15 Un - fortunately, treatment recommendations are based almost entirely on non-randomized clinical trials. Only one small randomized trial has been conducted. 16 Thus, most of the recommendations here are based on our experience and some larger published retrospective series. Early treatment of RSV upper respiratory tract infection has been advocated by several experts, 1 especially in the presence of lymphopenia (which is a significant risk factor for progression) or in other high risk situations. 17 This strategy was moderately effective in one large retrospective review. 18 The data suggest that treatment of early pneumonia (i.e., prior to mechanical ventilation) is associated with improved outcome. | 330 | Hematology Education: the education programme for the annual congress of the European Hematology Association | 2011; 5(1)
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H e m a t o l o g y E d u c a t i o
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Copyright Information ©2011 by Eur
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Editorial Board Education Book Edit
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Acute lymphoblastic leukemia 1-8 Th
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S. Schnell P. Van Vlierberghe A. Fe
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lineage cells, and in differentiati
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FLT3 mutations The FMS-like tyrosin
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44. Bar-Eli M, Ahuja H, Foti A, Cli
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J.M. Rowe 1,2 C. Ganzel 1 1 Shaare
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treated on the MRC UKALL XII/ECOG29
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asparaginase (PEG), where the Esche
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or higher. It is, however, importan
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25. Bruggemann M, Schrauder A, Raff
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lymphoblastic leukemia: prospective
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such as high white blood cell count
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doxorubicine, there was a trend tow
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of the aging process with respect t
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K.L. Rice 1 M. Buzzai 2 J. Altman 1
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ing FLT3-ITD, wild-type NPM1, or bo
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ciated with gene activation, via th
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leukemia with inv(16) and t(8;21):
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99. Parsons DW, Jones S, Zhang X, e
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abnormalities, some of which are al
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file. 27,31 Thus, the double gene-m
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karyotype represents a distinct gen
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Table 1. Meta-analysis of 23 random
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A recent study by the Center for In
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Patients with HLA-matched related o
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After allogeneic HSCT, an autologou
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A. Bacigalupo Ospedale San Martino,
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Table 2. The effect of HLA mismatch
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References 1. Petersdorf EW, Malkki
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neutrophil and platelet recovery an
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Figure 2. One Year-Overall Survival
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infused on day 21. No serious adver
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W, et al. Effect of graft source on
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TRM was higher for patients who rec
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following a myeloablative preparati
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effect. Surprisingly, none of the p
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nancies. Bone Marrow Transplant. 20
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J.G. Gilles Center for Molecular an
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14C12 was humanized by grafting VH
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Table 1. VWD Classification. VWD Su
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Figure 1. Missense mutations found
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associated with an increased bleedi
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49. Brown SA, Eldridge A, Collins P
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leed. These issues are especially i
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estored function. 43,44 A phase I t
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years’ experience of prophylactic
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J.A. Burger Department of Leukemia,
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chemotaxis, migration across vascul
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Regulatory T cells (T reg), identif
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16. Burger JA, Ghia P, Rosenwald A,
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TE, Nowakowski GS, et al. CD49d exp
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andomized trial demonstrating impro
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Conclusions Chemoimmunotherapy has
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with multiple comorbidities (≥ 2)
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ment was finished in all 100 patien
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Table 2. Treatment recommendation f
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34. Ferrajoli A. The combination of
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to be the source of additional gene
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potential to prevent LSCs from acce
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ABL1 confirms that eradication of d
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65. Fiskus W, Pranpat M, Balasis M,
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alive after 10 years. 11 Hence, CCy
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each arm). A minimal change in myel
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Any discussion about the definition
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H. Kantarjian J. Cortes Leukemia De
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59%; the CCyR rate was 44%. Among p
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ern era of BCR-ABL1 tyrosine kinase
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the hematopoietic system, 10 nor in
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over the period of 6 weeks, demonst
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Data on clonal changes in the blood
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2006 Feb 1;107(3):924-30. 41. Liang
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demonstrated that changes in osteob
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“Mafia” transgenic mice in whic
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68. Coetzee T, Fujita N, Dupree J,
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ization. In WASP deficiency, lympho
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Currently the epistatic relationshi
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R. Küppers Institute of Cell Biolo
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Figure 1. TNFAIP3 mutation in HL ce
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Figure 2. HRS cells and their precu
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Hansmann ML, et al. Detection of cl
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fying patients for whom different a
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prognosis HL, whilst those with res
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12. Noordijk EM, Carde P, Dupouy N,
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A. Sureda Consultant in Haematology
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Figure 1. Long-term outcome of pati
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from a MRD and 18 from MUDs. All pa
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Parker PM, Stein AS, et al. High-do
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R. Stasi Department of Haematology,
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common variants in the regulatory r
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against the TPO receptor (cMpl). 61
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W.B. Mitchell A.A. Miller J.B. Buss
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platelet counts and/or bleeding. Th
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Mpl. Cell. 1994;77(7):1117-24. 6. d
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ity and mortality associated with t
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to azathioprine, and is particularl
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stemming from antibodies against PE
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L. Pasqualucci Institute for Cancer
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cation of molecularly distinct subg
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of cases) 46 and amplifications of
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gene alterations in B cell lymphoma
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W. Wilson National Cancer Institute
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clear distinction among the lymphom
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Treatment strategies in germinal ce
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in ABC DLBCL (Hernandez et al., 201
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DLBCL that mostly occurs in young p
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phoma. J Clin Oncol. 2005;23:5347-5
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Table 1. Diffuse Large B cell Lymph
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sion/relapse are similar to those i
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intensive therapy with curative int
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A. Karsan Genome Sciences Centre an
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Balanced translocations In contrast
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some arm 5q have also been implicat
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(H3K27) methyltransferase, and is a
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38. Starczynowski DT, Morin R, McPh
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G. Garcia-Manero Department of Leuk
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trial evaluating different doses an
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acid. 62 The second was a large mul
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Borthakur G, et al. Cause of death
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P. Krishnamurthy 1 G.J. Mufti 1,2 1
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etween 1995 and 2005. 11 Five hundr
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London, United Kingdom, June 9-12,
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attainment of FDC post DLI. Interes
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myelodysplastic syndromes is associ
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ubiquitous chaperone that promotes
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was thought that they are linked to
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pathologic induction of miR-28 in M
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STATs. Second, levels of HP1 alpha
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72. Irandoust MI, Aarts LH, Roovers
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A.M. Vannucchi Section of Hematolog
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2,559 patients with a diagnosis of
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tant use of aspirin should be caref
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sions at this regard. Based on thes
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in bcr-abl-negative myeloproliferat
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Table 1. Prognostic scoring systems
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Figure 1. Current inhibitors of JAK
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Table 4. A risk-based approach to d
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the flexibility to be adjusted as t
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A. Vacca 1 D. Ribatti 2 1 Departmen
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neovessel building together with MM
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Mevastatin, a specific inhibitor of
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Page 292 and 293: Genetics prognostic tools should be
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Page 296 and 297: Table 1. Conventional chemotherapy
Page 298 and 299: Novel agents given as consolidation
Page 300 and 301: dence of peripheral neuropathy, gas
Page 302 and 303: 31. Barlogie B, Tricot G, Anaissie
Page 304 and 305: Table 1. Major differences between
Page 306 and 307: first line therapy have shown survi
Page 308 and 309: transplantation, 7,91 and generally
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Page 312 and 313: Table 1. Clinical signs of possible
Page 314 and 315: Table 4. Distribution of CSF involv
Page 316 and 317: ently results in a less than 5% cum
Page 318 and 319: 90. German-Austrian-Swiss ALL-BFM S
Page 320 and 321: U. Nowak-Göttl 1 R. Junker 1 A. Kr
Page 322 and 323: Based on the data obtained from the
Page 324 and 325: 59. Male C, Chait P, Ginsberg JS, e
Page 326 and 327: Table 1. Characteristic features of
Page 328 and 329: Table 2. Mutational spectrum of CDA
Page 330 and 331: megarakaryoblastic leukemia (AMKL)
Page 332 and 333: R.E. Ware Professor and Vice-Chairm
Page 334 and 335: protein, cytokines, and soluble adh
Page 336 and 337: example, improving blood viscosity
Page 340 and 341: London, United Kingdom, June 9-12,
Page 342 and 343: port have also been used. 5 Combina
Page 344 and 345: Wingard JR, Young J-AH, Boeckh MJ.
Page 346 and 347: K. Rezvani 1 J. Barrett 2 1 Haemato
Page 348 and 349: include the childhood infectious il
Page 350 and 351: Summary Patients undergoing hematop
Page 352 and 353: Table 1. Key issues. In a retrospec
Page 354 and 355: invasive method to assess iron over
Page 356 and 357: stitution but even with optimal sub
Page 358 and 359: T.M. Hackeng Department of Biochemi
Page 360 and 361: and inhibits FVIIa, and that the se
Page 362 and 363: Figure 4. Regulation of coagulation
Page 364 and 365: T. Baglin Department of Haematology
Page 366 and 367: Figure 1. Illustration of alternati
Page 368 and 369: compared with 3.5% in patients with
Page 370 and 371: 49. Hron G, Kollars M, Binder BR, E
Page 372 and 373: Women receiving vitamin K antagonis
Page 374 and 375: molecular weight heparin as prophyl
Page 376 and 377: eral morbidity and mortality. 17-21
Page 378 and 379: the HOD construct. Furthermore, the
Page 380 and 381: Goals of future murine studies incl
Page 382 and 383: F. Noizat-Pirenne C. Tournamille Et
Page 384 and 385: phenotype. 26 In 2010, we investiga
Page 386 and 387: ody has been involved in DHTR. 37 T
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antigen. Cases can be encountered d
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S.R. Sloan Harvard Medical School &
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We also analyzed patient databases
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Index of authors Altman J. 27 Bacig
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Cornelissen J. Affiliations to disc
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GlaxoSmithKline (Research Support;
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