H e m a t o lo g y E d u c a t io n - European Hematology Association

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72. Irandoust MI, Aarts LH, Roovers O, Gits J, Erkeland SJ, Touw IP. Suppressor of cytokine signaling 3 controls lysosomal routing of G-CSF receptor. EMBO J. 2007 Apr 4;26(7):1782-93. 73. Wang Q, Miyakawa Y, Fox N, Kaushansky K. Interferonalpha directly represses megakaryopoiesis by inhibiting thrombopoietin-induced signaling through induction of SOCS-1. Blood. 2000 Sep 15;96(6):2093-9. 74. Chaligne R, Tonetti C, Besancenot R, Marty C, Kiladjian JJ, Socie G, et al. SOCS3 inhibits TPO-stimulated, but not spontaneous, megakaryocytic growth in primary myelofibrosis. Leukemia. 2009 Jun;23(6):1186-90. 75. Teofili L, Martini M, Cenci T, Guidi F, Torti L, Giona F, et al. Epigenetic alteration of SOCS family members is a possible pathogenetic mechanism in JAK2 wild type myeloproliferative diseases. Int J Cancer. 2008 Oct 1;123(7):1586-92. 76. Jost E, do ON, Dahl E, Maintz CE, Jousten P, Habets L, et al. Epigenetic alterations complement mutation of JAK2 tyrosine kinase in patients with BCR/ABL-negative myeloproliferative disorders. Leukemia. 2007 Mar;21(3):505-10. 77. Haan S, Wuller S, Kaczor J, Rolvering C, Nocker T, Behrmann I, et al. SOCS-mediated downregulation of mutant Jak2 (V617F, T875N and K539L) counteracts cytokine-independent signaling. Oncogene. 2009 Aug 27;28(34):3069-80. 78. Hookham MB, Elliott J, Suessmuth Y, Staerk J, Ward AC, Vainchenker W, et al. The myeloproliferative disorder-associated JAK2 V617F mutant escapes negative regulation by suppressor of cytokine signaling 3. Blood. 2007 Jun 1;109(11):4924-9. 79. Elliott J, Suessmuth Y, Scott LM, Nahlik K, McMullin MF, Constantinescu SN, et al. SOCS3 tyrosine phosphorylation as a potential bio-marker for myeloproliferative neoplasms associated with mutant JAK2 kinases. Haematologica. 2009 Apr;94(4):576-80. 80. Quentmeier H, Geffers R, Jost E, Macleod RA, Nagel S, Rohrs S, et al. SOCS2: inhibitor of JAK2V617F-mediated signal transduction. Leukemia. 2008 Dec;22(12):2169-75. 81. Tannahill GM, Elliott J, Barry AC, Hibbert L, Cacalano NA, Johnston JA. SOCS2 can enhance interleukin-2 (IL-2) and IL- 3 signaling by accelerating SOCS3 degradation. Mol Cell Biol. 2005 Oct;25(20):9115-26. 82. Stein BL, Williams DM, Rogers O, Isaacs MA, Spivak JL, Moliterno AR. Disease burden at the progenitor level is a feature of primary myelofibrosis: a multivariable analysis of 164 JAK2 V617F-positive myeloproliferative neoplasm patients. Exp Hematol. 2011 Jan;39(1):95-101. 83. James C, Mazurier F, Dupont S, Chaligne R, Lamrissi-Garcia I, Tulliez M, et al. The hematopoietic stem cell compartment of JAK2V617F-positive myeloproliferative disorders is a reflection of disease heterogeneity. Blood. 2008 Sep 15;112(6):2429-38. 84. Bumm TG, Elsea C, Corbin AS, Loriaux M, Sherbenou D, Wood L, et al. Characterization of murine JAK2V617F-positive myeloproliferative disease. Cancer Res. 2006 Dec 1;66 (23):11156-65. 85. Bumm TGP, VanDyke J, Loriaux M, Gendron C, Wood LG, Druker BJ, et al. TNF-alpha plays a crucial role in the JAK2- V617F induced myeloproliferative disorder. Blood. 2007; 110:Abstract 675. 86. Van Pelt K, Nollet F, Selleslag D, Knoops L, Constantinescu SN, Criel A, et al. The JAK2V617F mutation can occur in a hematopoietic stem cell that exhibits no proliferative advantage: a case of human allogeneic transplantation. Blood. 2008 Aug 1;112(3):921-2. 87. Li J, Spensberger D, Ahn JS, Anand S, Beer PA, Ghevaert C, et al. JAK2 V617F impairs hematopoietic stem cell function in a conditional knock-in mouse model of JAK2 V617F-positive essential thrombocythemia. Blood. 2010 Sep 2;116(9):1528-38. 88. Dykstra B, Kent D, Bowie M, McCaffrey L, Hamilton M, Lyons K, et al. Long-term propagation of distinct hematopoietic differentiation programs in vivo. Cell Stem Cell. 2007 Aug 16;1(2):218-29. 89. Muller-Sieburg CE, Cho RH, Karlsson L, Huang JF, Sieburg HB. Myeloid-biased hematopoietic stem cells have extensive self-renewal capacity but generate diminished lymphoid progeny with impaired IL-7 responsiveness. Blood. 2004 Jun 1;103(11):4111-8. 90. Challen GA, Boles NC, Chambers SM, Goodell MA. Distinct hematopoietic stem cell subtypes are differentially regulated by TGF-beta1. Cell Stem Cell. 2010 Mar 5;6(3):265-78. 91. Chagraoui H, Komura E, Tulliez M, Giraudier S, Vainchenker W, Wendling F. Prominent role of TGF-beta 1 in thrombopoietin-induced myelofibrosis in mice. Blood. 2002 Nov 15; 100(10):3495-503. 92. Tiedt R, Hao-Shen H, Sobas MA, Looser R, Dirnhofer S, Schwaller J, et al. Ratio of mutant JAK2-V617F to wild-type London, United Kingdom, June 9-12, 2011 Jak2 determines the MPD phenotypes in transgenic mice. Blood. 2008 Apr 15;111(8):3931-40. 93. Lacout C, Pisani DF, Tulliez M, Moreau Gachelin F, Vainchenker W, Villeval JL. JAK2V617F expression in murine hematopoietic cells leads to MPD mimicking human PV with secondary myelofibrosis. Blood. 2006 May 2;108:1652-60. 94. Wernig G, Mercher T, Okabe R, Levine RL, Lee BH, Gilliland DG. Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model. Blood. 2006 Jun 1;107(11):4274-81. 95. Zaleskas VM, Krause DS, Lazarides K, Patel N, Hu Y, Li S, et al. Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617F. PLoS ONE. 2006;1:e18. 96. Marty C, Lacout C, Martin A, Hasan S, Jacquot S, Birling MC, et al. Myeloproliferative neoplasm induced by constitutive expression of JAK2V617F in knock-in mice. Blood. 2010 Aug 5;116(5):783-7. 97. Xing S, Wanting TH, Zhao W, Ma J, Wang S, Xu X, et al. Transgenic expression of JAK2V617F causes myeloproliferative disorders in mice. Blood. 2008 May 15;111(10):5109-17. 98. Pardanani A, Fridley BL, Lasho TL, Gilliland DG, Tefferi A. Host genetic variation contributes to phenotypic diversity in myeloproliferative disorders. Blood. 2008 Mar 1;111(5):2785-9. 99. Villeval JL, Cohen-Solal K, Tulliez M, Giraudier S, Guichard J, Burstein SA, et al. High thrombopoietin production by hematopoietic cells induces a fatal myeloproliferative syndrome in mice. Blood. 1997 Dec 1;90(11):4369-83. 100. Thiele J, Kvasnicka HM. A critical reappraisal of the WHO classification of the chronic myeloproliferative disorders. Leuk Lymphoma. 2006 Mar;47(3):381-96. 101. Ciurea SO, Merchant D, Mahmud N, Ishii T, Zhao Y, Hu W, et al. Pivotal contributions of megakaryocytes to the biology of idiopathic myelofibrosis. Blood. 2007 Aug 1;110(3):986-93. 102. Thiele J, Holgado S, Choritz H, Georgii A. Abnormalities of megakaryocytes in myelitis and chronic myeloproliferative diseases. Virchows Arch B Cell Pathol Incl Mol Pathol. 1982; 41(1-2):67-81. 103. Bernard OA, Delhommeau F, Fontenay M, Vainchenker W. [Mutations in TET2 in myeloid cancers]. Med Sci (Paris). 2009 Oct;25(10):785-8. 104. Delhommeau F, Dupont S, Della Valle V, James C, Trannoy S, Masse A, et al. Mutation in TET2 in myeloid cancers. N Engl J Med. 2009 May 28;360(22):2289-301. 105. Tefferi A, Pardanani A, Lim KH, Abdel-Wahab O, Lasho TL, Patel J, et al. TET2 mutations and their clinical correlates in polycythemia vera, essential thrombocythemia and myelofibrosis. Leukemia. 2009 May;23(5):905-11. 106. Chen E, Beer PA, Godfrey AL, Ortmann CA, Li J, Costa- Pereira AP, et al. Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signaling. Cancer Cell. 2010 Nov 16;18(5):524-35. 107. Najean Y, Rain JD. The very long-term evolution of polycythemia vera: an analysis of 318 patients initially treated by phlebotomy or 32P between 1969 and 1981. Semin Hematol. 1997 Jan;34(1):6-16. 108. Mesa RA, Li CY, Ketterling RP, Schroeder GS, Knudson RA, Tefferi A. Leukemic transformation in myelofibrosis with myeloid metaplasia: a single-institution experience with 91 cases. Blood. 2005 Feb 1;105(3):973-7. 109. Plo I, Nakadake M, Malivert L, de Villartay JP, Giraudier S, Villeval J-L, Wiesmuller L Vainchenker W. JAK2 stimulates homologous recombination and genetic instability: potential implication in the heterogeneity of myeloproliferative disorders. Blood. 2008 Aug15;112(4):1402-12. 110. Beer PA, Ortmann CA, Stegelmann F, Guglielmelli P, Reilly JT, Larsen TS, et al. Molecular mechanisms associated with leukemic transformation of MPL-mutant myeloproliferative neoplasms. Haematologica. 2010 Dec;95(12):2153-6. 111. Pardanani A, Lasho TL, Finke CM, Mai M, McClure RF, Tefferi A. IDH1 and IDH2 mutation analysis in chronic- and blast-phase myeloproliferative neoplasms. Leukemia. 2010 Jun;24(6):1146-51. 112. Jager R, Gisslinger H, Passamonti F, Rumi E, Berg T, Gisslinger B, et al. Deletions of the transcription factor Ikaros in myeloproliferative neoplasms. Leukemia. 2010 Jul;24(7):1290-8. 113. Haferlach C, Dicker F, Herholz H, Schnittger S, Kern W, Haferlach T. Mutations of the TP53 gene in acute myeloid leukemia are strongly associated with a complex aberrant karyotype. Leukemia. 2008 Aug;22(8):1539-41. 114. Dang L, Jin S, Su SM. IDH mutations in glioma and acute myeloid leukemia. Trends Mol Med. 2010 Sep;16(9):387-97. 115. Georgopoulos K. Haematopoietic cell-fate decisions, chromatin regulation and ikaros. Nat Rev Immunol. 2002 Mar; 2(3):162-74. Hematology Education: the education programme for the annual congress of the European Hematology Association | 2011; 5(1) | 253 |
16 th Congress of the European Hematology Association 116. Harada Y, Harada H. Molecular pathways mediating MDS/AML with focus on AML1/RUNX1 point mutations. J Cell Physiol. 2009 Jul;220(1):16-20. 117. Shi S, Calhoun HC, Xia F, Li J, Le L, Li WX. JAK signaling globally counteracts heterochromatic gene silencing. Nat Genet. 2006;38(9):1071-6. 118. Shi S, Larson K, Guo D, Lim SJ, Dutta P, Yan SJ, et al. Drosophila STAT is required for directly maintaining HP1 localization and heterochromatin stability. Nat Cell Biol. 2008 Apr;10(4):489-96. 119. Dawson MA, Bannister AJ, Gottgens B, Foster SD, Bartke T, Green AR, et al. JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatin. Nature. 2009 Oct 8;461(7265):819-22. 120. Griffiths DS, Li J, Dawson MA, Trotter MW, Cheng YH, Smith AM, et al. LIF-independent JAK signalling to chromatin in embryonic stem cells uncovered from an adult stem cell disease. Nat Cell Biol. 2010 Jan;13(1):13-21. 121. Onishi M, Nosaka T, Misawa K, Mui AL, Gorman D, McMahon M, et al. Identification and characterization of a constitutively active STAT5 mutant that promotes cell proliferation. Mol Cell Biol. 1998;18(7):3871-9. 122. Liu F, Zhao X, Perna F, Wang L, Koppikar P, Abdel-Wahab O, et al. JAK2V617F-Mediated Phosphorylation of PRMT5 Downregulates Its Methyltransferase Activity and Promotes Myeloproliferation. Cancer Cell. 2011 Feb 15;19(2):283-94. | 254 | 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
Page 212 and 213: Treatment strategies in germinal ce
Page 214 and 215: in ABC DLBCL (Hernandez et al., 201
Page 216 and 217: DLBCL that mostly occurs in young p
Page 218 and 219: phoma. J Clin Oncol. 2005;23:5347-5
Page 220 and 221: Table 1. Diffuse Large B cell Lymph
Page 222 and 223: sion/relapse are similar to those i
Page 224 and 225: intensive therapy with curative int
Page 226 and 227: A. Karsan Genome Sciences Centre an
Page 228 and 229: Balanced translocations In contrast
Page 230 and 231: some arm 5q have also been implicat
Page 232 and 233: (H3K27) methyltransferase, and is a
Page 234 and 235: 38. Starczynowski DT, Morin R, McPh
Page 236 and 237: G. Garcia-Manero Department of Leuk
Page 238 and 239: trial evaluating different doses an
Page 240 and 241: acid. 62 The second was a large mul
Page 242 and 243: Borthakur G, et al. Cause of death
Page 244 and 245: P. Krishnamurthy 1 G.J. Mufti 1,2 1
Page 246 and 247: etween 1995 and 2005. 11 Five hundr
Page 248 and 249: London, United Kingdom, June 9-12,
Page 250 and 251: attainment of FDC post DLI. Interes
Page 252 and 253: myelodysplastic syndromes is associ
Page 254 and 255: ubiquitous chaperone that promotes
Page 256 and 257: was thought that they are linked to
Page 258 and 259: pathologic induction of miR-28 in M
Page 260 and 261: STATs. Second, levels of HP1 alpha
Page 264 and 265: A.M. Vannucchi Section of Hematolog
Page 266 and 267: 2,559 patients with a diagnosis of
Page 268 and 269: tant use of aspirin should be caref
Page 270 and 271: sions at this regard. Based on thes
Page 272 and 273: in bcr-abl-negative myeloproliferat
Page 274 and 275: Table 1. Prognostic scoring systems
Page 276 and 277: Figure 1. Current inhibitors of JAK
Page 278 and 279: Table 4. A risk-based approach to d
Page 280 and 281: the flexibility to be adjusted as t
Page 282 and 283: A. Vacca 1 D. Ribatti 2 1 Departmen
Page 284 and 285: neovessel building together with MM
Page 286 and 287: Mevastatin, a specific inhibitor of
Page 288 and 289: egression of tumor vessels, and app
Page 290 and 291: diagnosis does not require genetic
Page 292 and 293: Genetics prognostic tools should be
Page 294 and 295: sone induction improves outcome of
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
Page 310 and 311: methylation characterizes juvenile
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Table 1. Clinical signs of possible
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Table 4. Distribution of CSF involv
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ently results in a less than 5% cum
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90. German-Austrian-Swiss ALL-BFM S
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U. Nowak-Göttl 1 R. Junker 1 A. Kr
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Based on the data obtained from the
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59. Male C, Chait P, Ginsberg JS, e
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Table 1. Characteristic features of
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Table 2. Mutational spectrum of CDA
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megarakaryoblastic leukemia (AMKL)
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R.E. Ware Professor and Vice-Chairm
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protein, cytokines, and soluble adh
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example, improving blood viscosity
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92(9):1266-7. 36. Bensinger TA, Gil
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London, United Kingdom, June 9-12,
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port have also been used. 5 Combina
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Wingard JR, Young J-AH, Boeckh MJ.
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K. Rezvani 1 J. Barrett 2 1 Haemato
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include the childhood infectious il
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Summary Patients undergoing hematop
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Table 1. Key issues. In a retrospec
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invasive method to assess iron over
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stitution but even with optimal sub
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T.M. Hackeng Department of Biochemi
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and inhibits FVIIa, and that the se
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Figure 4. Regulation of coagulation
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T. Baglin Department of Haematology
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Figure 1. Illustration of alternati
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compared with 3.5% in patients with
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49. Hron G, Kollars M, Binder BR, E
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Women receiving vitamin K antagonis
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molecular weight heparin as prophyl
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eral morbidity and mortality. 17-21
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the HOD construct. Furthermore, the
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Goals of future murine studies incl
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F. Noizat-Pirenne C. Tournamille Et
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phenotype. 26 In 2010, we investiga
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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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