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sone induction improves outcome of patients with t(4;14) myeloma but not outcome of patients with del(17p). J Clin Oncol. 2010 Oct 20;28(30):4630-4. 32. Zandecki M, Lai JL, Genevieve F, Bernardi F, Volle-Remy H, Blanchet O, et al. Several cytogenetic subclones may be identified within plasma cells from patients with monoclonal gammopathy of undetermined significance, both at diagnosis and during the indolent course of this condition. Blood. 1997;90(9): 3682-90. 33. Avet-Loiseau H, Facon T, Daviet A, Godon C, Rapp MJ, Harousseau JL, et al. 14q32 translocations and monosomy 13 observed in monoclonal gammopathy of undetermined significance delineate a multistep process for the oncogenesis of multiple myeloma. Intergroupe Francophone du Myelome. Cancer Res. 1999;59(18):4546-50. 34. Fonseca R, Bailey RJ, Ahmann GJ, Rajkumar SV, Hoyer JD, Lust JA, et al. Genomic abnormalities in monoclonal gammopathy of undetermined significance. Blood. 2002 July 30; 100(4):1417-24. 35. Smadja NV, Fruchart C, Isnard F, Louvet C, Dutel JL, Cheron N, et al. Chromosomal analysis in multiple myeloma: cytogenetic evidence of two different diseases. Leukemia. 1998; 12(6):960-9. 36. Fonseca R, Debes-Marun CS, Picken EB, Dewald GW, Bryant SC, Winkler JM, et al. The recurrent IgH translocations are highly associated with nonhyperdiploid variant multiple myeloma. Blood. 2003 Oct 1;102(7):2562-2567. 37. Debes-Marun C, Dewald G, Bryant S, Picken E, Santana- Dávila S, González-Paz N, et al. Chromosome abnormalities clustering and its implications for pathogenesis and prognosis in myeloma. Leukemia. 2003 February;17(2):427-436. 38. Ross FM, Ibrahim AH, Vilain-Holmes A, Winfield MO, Chiecchio L, Protheroe RK, et al. Age has a profound effect on the incidence and significance of chromosome abnormalities in myeloma. Leukemia. 2005 Sep;19(9):1634-42. 39. Drach J, Ackermann J, Kromer E, Fritz E, Schuster R, Gisslinger H, et al. Short survival of Patients with Multpile Myeloma and p53 gene deletion: A study by Interphase FISH. Blood. 1997; 90:244a. 40. Jagannath S, Richardson PG, Sonneveld P, Schuster MW, Irwin D, Stadtmauer EA, et al. Bortezomib appears to overcome the poor prognosis conferred by chromosome 13 deletion in phase 2 and 3 trials. Leukemia. 2007 Jan;21(1):151-7. 41. San Miguel JF, Schlag R, Khuageva NK, Dimopoulos MA, Shpilberg O, Kropff M, et al. Bortezomib plus melphalan and prednisone for initial treatment of multiple myeloma. N Engl J Med. 2008 Aug 28;359(9):906-17. 42. Richardson P. Optimizing bortezomib treatment in patients with relapsed multiple myeloma. Clin Adv Hematol Oncol. 2006 May;4(5):4-5. 43. Kapoor P, Kumar S, Fonseca R, Lacy MQ, Witzig TE, Hayman SR, et al. Impact of risk stratification on outcome among patients with multiple myeloma receiving initial therapy with lenalidomide and dexamethasone. Blood. 2009 Jul 16;114(3): 518-21. 44. Reece D, Song KW, Fu T, Roland B, Chang H, Horsman DE, et al. Influence of cytogenetics in patients with relapsed or refractory multiple myeloma treated with lenalidomide plus dexamethasone: adverse effect of deletion 17p13. Blood. 2009 Jul 16;114(3):522-525. 45. Avet-Loiseau H, Soulier J, Fermand JP, Yakoub-Agha I, Attal M, Hulin C, et al. Impact of high-risk cytogenetics and prior therapy on outcomes in patients with advanced relapsed or refractory multiple myeloma treated with lenalidomide plus dexamethasone. Leukemia. 2010 Mar; 24(3): 623-8. 46. Keats JJ, Fonseca R, Chesi M, Schop R, Baker A, Chng WJ, et al. Promiscuous mutations activate the noncanonical NFkappaB pathway in multiple myeloma. Cancer Cell. 2007 Aug;12(2):131-44. 47. Chng WJ, Price-Troska T, Gonzalez-Paz N, Van Wier S, Jacobus S, Blood E, et al. Clinical significance of TP53 mutation in myeloma. Leukemia. 2007 Mar;21(3):582-4. London, United Kingdom, June 9-12, 2011 48. Drach J, Ackermann J, Fritz E, Kromer E, Schuster R, Gisslinger H, et al. Presence of a p53 gene deletion in patients with multiple myeloma predicts for short survival after conventionaldose chemotherapy. Blood. 1998;92(3):802-809. 49. Chang H, Qi C, Yi QL, Reece D, Stewart AK. p53 gene deletion detected by fluorescence in situ hybridization is an adverse prognostic factor for patients with multiple myeloma following autologous stem cell transplantation. Blood. 2005 Jan 1;105(1):358-60. 50. Xiong W, Wu X, Starnes S, Johnson SK, Haessler J, Wang S, et al. An analysis of the clinical and biologic significance of TP53 loss and the identification of potential novel transcriptional targets of TP53 in multiple myeloma. Blood. 2008 Nov 15;112(10):4235-46. 51. Kapoor P, Fonseca R, Rajkumar SV, Sinha S, Gertz MA, Stewart AK, et al. Evidence for cytogenetic and fluorescence in situ hybridization risk stratification of newly diagnosed multiple myeloma in the era of novel therapie. Mayo Clin Proc 2010 Jun;85(6):532-7. 52. Keats JJ, Reiman T, Maxwell CA, Taylor BJ, Larratt LM, Mant MJ, et al. In multiple myeloma, t(4;14)(p16;q32) is an adverse prognostic factor irrespective of FGFR3 expression. Blood. 2003;101(4):1520-9. 53. Chng WJ, Jacobus S, Fonseca R. Do beta2 microglobulin levels affect survival of newly diagnosed myeloma patients with translocation t(4;14) or 17p13 deletion treated with conventional chemotherapy? Leukemia. 2008;May22(5):1080-1. Epub 2007 Nov 29. 54. Chng WJ, Kuehl WM, Bergsagel PL, Fonseca R. Translocation t(4;14) retains prognostic significance even in the setting of high-risk molecular signature. Leukemia. 2008 Feb;22(2):459- 61. Epub 2007 Sep 6. 55. Ross FM, Chiecchio L, Dagrada G, Protheroe RK, Stockley DM, Harrison CJ, et al. The t(14;20) is a poor prognostic factor in myeloma but is associated with long term stable disease in MGUS. Haematologica. 2010 Jul;95(7):1221-5. Epub 2010 Apr 21. 56. Avet-Loiseau H, Malard F, Campion L, Magrangeas F, Sebban C, Lioure B, et al. Translocation t(14;16) and multiple myeloma: is it really an independent prognostic factor? Blood. 2011 Feb 10;117(6):2009-11. Epub 2010 Oct 20. 57. Chang H, Ning Y, Qi X, Yeung J, Xu W. Chromosome 1p21 deletion is a novel prognostic marker in patients with multiple myeloma. Br J Haematol 2007 Oct 1;139(1):51-4. 58. Chang H, Qi X, Yeung J, Reece D, Xu W, Patterson B. Genetic aberrations including chromosome 1 abnormalities and clinical features of plasma cell leukemia. Leuk Res. 2009 Feb 1;33(2):259-62. 59. Chang H, Qi X, Jiang A, Xu W, Young T, Reece D. 1p21 deletions are strongly associated with 1q21 gains and are an independent adverse prognostic factor for the outcome of highdose chemotherapy in patients with multiple myeloma. Bone Marrow Transplant. 2010 Jan 1;45(1):117-121. 60. Chang H, Jiang N, Jiang H, Saha M, Qi C, Xu W, et al. CKS1B nuclear expression is inversely correlated with p27Kip1 expression and is predictive of an adverse survival in multiple myeloma. Haematologica. 2010 Sep;95(9):1620. 61. Zhan F, Colla S, Wu X, Chen B, Stewart JP, Kuehl WM, et al. CKS1B, over expressed in aggressive disease, regulates multiple myeloma growth and survival through SKP2- and p27Kip1-dependent and independent mechanisms. Blood. 2007 Jun 1;109(11):4995-5001. Epub 2007 Feb 15. 62. Neri A, Baldini L, Trecca D, Cro L, Polli E, Maiolo AT. p53 gene mutations in multiple myeloma are associated with advanced forms of malignancy. Blood. 1993;81(1):128-35. 63. Liu P, Leong T, Quam L, Billadeau D, Kay NE, Greipp P, et al. Activating mutations of N- and K-ras in multiple myeloma show different clinical associations: analysis of the Eastern Cooperative Oncology Group Phase III Trial. Blood. 1996;88(7):2699-2706. Hematology Education: the education programme for the annual congress of the European Hematology Association | 2011; 5(1) | 285 |
P. Moreau Hematology Department, University Hospital Hôtel-Dieu, Ricordeau, France Hematology Education: the education program for the annual congress of the European Hematology Association 2011;5:286-293 Multiple myeloma Frontline treatment of multiple myeloma Introduction The decision to treat a patient is based on the criteria set for the diagnosis of symptomatic multiple myeloma (MM), which includes the CRAB (hypocalcaemia, renal dysfunction, anemia, and bone lesions) criteria. Patients with clearly defined monoclonal gammapathy of unknown significance (MGUS) or smoldering multiple myeloma (SMM) do not need initiation of therapy irrespective of any associated risk factors except specifically targeted protocols. 1 Treatment of patients less than 66 years of age Autologous stem cell transplantation ASCT versus conventional chemotherapy CC A key therapeutic advance was the introduction almost 25 years ago of high-dose melphalan therapy supported by autologous hematopoietic stem-cell transplantation. 2 The Intergroupe Francophone du Myelome was the first to conduct a randomized trial showing the superiority of this approach compared with CC in terms of response rate, event-free survival (EFS), and overall survival (OS). 3 These results were confirmed 7 years later by the British Medical Research Council. 4 As a consequence of these two studies, ASCT became the standard of care for frontline therapy, at least in younger patients (up to 65 years of age) with normal renal function. An important finding from these studies was a significant increase in the rate of CR (negative immunofixation) or very good partial remission (reduction of the M-component by more than 90%) with ASCT, which was significantly correlated with longer progression-free survival (PFS) and OS. Overall, the use of ASCT did improve the median OS from 3 years to 50 to 55 months. The results of randomized trials comparing conventional chemotherapy A B S T R A C T This review will focus on the current frontline treatment of multiple myeloma. High-dose therapy and autologous stem cell transplantation in younger patients, and new treatment modalities including the use of novel agents in elderly patients will be discussed. to high-dose therapy and ASCT are summarized (Table 1). The clinical results of HDT were obtained with two types of conditioning regimens, using either high-dose melphalan alone or regimen additionally containing total-body irradiation (TBI). The IFM group compared melphalan 200 mg/m² (Mel200) and melphalan 140 mg/m² plus 8 Gy TBI and showed that Mel200 was at least as effective and better tolerated than the regimen containing TBI. 10 Moreover, while EFS was identical in both groups, OS was significantly longer with Mel200 due to a longer OS after first relapse. As a result, Mel200 became the preferred preparative regimen, and up to now, no randomized trial has shown the superiority of any other conditioning regimen compared with Mel200. Tandem transplantation Strategies based on further intensification were explored with the aim of improving on the results obtained with single ASCT. The IFM was the first to conduct a randomized trial comparing single and double ASCT in 599 patients up to 60 years of age. 11 On an intent-to-treat basis, the 7-year EFS and OS were significantly improved in the double ASCT arm. The benefit for EFS, but not for OS was confirmed by two other randomized studies (Table 2). 12,13 All three published studies showed that achievement of CR (or at least a VGPR) had a favorable impact on EFS and/or OS. However, many investigators considered the benefit of this approach to be marginal, and were concerned by cost and morbidity. Therefore, defining which patients could derive benefit from this aggressive approach was important. The only parameter that predicted the patients who did or did not benefit from double ASCT was response to the first ASCT. Patients with less than 90% reduction of their M-component after one ASCT had a longer OS in the double ASCT arm, whereas patients achieving CR or VGPR after the first ASCT had the same OS with or without the | 286 | 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
Page 244 and 245: P. Krishnamurthy 1 G.J. Mufti 1,2 1
Page 246 and 247: etween 1995 and 2005. 11 Five hundr
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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
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Page 260 and 261: STATs. Second, levels of HP1 alpha
Page 262 and 263: 72. Irandoust MI, Aarts LH, Roovers
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
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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
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Page 292 and 293: Genetics prognostic tools should be
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
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 338 and 339: 92(9):1266-7. 36. Bensinger TA, Gil
Page 340 and 341: London, United Kingdom, June 9-12,
Page 342 and 343: 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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