12th Congress of the European Hematology ... - Haematologica

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12 th Congress of the European Hematology Association Novel therapeutics and targeted therapies I 0309 FUNCTIONAL CHARACTERISTICS AND GENE EXPRESSION PROFILES OF PRIMARY ACUTE MYELOID LEUKAEMIA CELLS IDENTIFY PATIENT SUBGROUPS THAT DIFFER IN THE SUSCEPTIBILITY TO HISTONE DEACETYLASE INHIBITORS C. Stapnes, 1 A. Ryningen, 1 K. Hatfield, 1 A.M. Oyan, 2 G.E. Eide, 3 K.H. Kalland, 2 B.T. Gjertsen, 1 O. Bruserud1 1 Institute of Medicine, BERGEN; 2 The Gade Institute, BERGEN; 3Centre for Clinical Research, BERGEN, Norway Modulation of gene expression through histone deacetylase (HDAC) inhibition is now considered a possible therapeutic strategy in several malignancies, including acute myeloid leukaemia (AML). In the present study we investigated the in vitro effects of various HDAC inhibitors on primary human AML cells. The relation between the biological response to HDAC inhibitors and basal gene expression profiles were assessed. AML cells were derived from 59 consecutive patients. Effects of structurally different HDAC inhibitors on cell proliferation, apoptosis induction, colony formation and CD34 cell subsets were studied. Basal gene expression of untreated cells was examined by microarray techniques. The HDAC inhibitors valproic acid, PXD101, trichostatin A and sodium butyrate were investigated. All drugs inhibited AML cell proliferation in a dose-dependent manner when tested at high concentrations. However, at lower concentrations, proliferation increased for a subset of patients. HDAC inhibitors also decreased proliferation of clonogenic and CD34 + leukaemic cells and increased apoptosis. Again the inhibition was observed at high concentrations whereas enhanced proliferation and decreased apoptosis were observed for a subset of patients at lower concentrations. Based on basal expression of 100 genes it was possible to separate patients (a group of 17 FLT3-ITD+ patients with normal cytogenetics) with growth enhancement at intermediate HDAC inhibitor concentrations and those without this response into two mutually exclusive groups. Several of the genes have previously been used for classification of AML patients. E.g. high expression of Dynein light chain 1 (DLC1) and low expression of transmembrane 4 superfamily member 2 (TM4SF2) has been associated with bad prognosis; DLC1 showed high expression in patients with drug-induced growth enhancement, whereas high TM4SF2 expression was observed for our group without growth enhancement. Low expression of members of the apolipoprotein system has been associated with adverse prognosis, and our patients with growth enhancement also showed low levels of Apolipoprotein C1 (APOC1). The two groups could not be separated on the basis of expression of HDACs and histone acetyl transferases. In conclusion, functional characterisation and gene expression analyses identify AML patient subsets that differ in their response to HDAC inhibitors in vitro. These observations may explain why HDAC inhibitor therapy affects only a subset of AML patients. 0310 TARGETED THERAPY OF ADULT T CELL LEUKEMIA: FROM THE BENCH TO BEDSIDE A. Bazarbachi, 1 R. Nasr, 1 M. El-Sabban, 1 H. El Hajj, 1 Y . Kfoury, 1 L. Haddad, 1 H. Hasegawa, 2 W. Hall, 2 H. De Thé, 3 O. Hermine4 1 American University of Beirut, BEIRUT, Lebanon; 2 University College Dublin, DUBLIN, Ireland; 3 UMR 7151 CNRS, PARIS, France; 4 Necker Hospital, PARIS, France Background. Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of mature activated T-cell caused by human T cell lymphotropic virus type I (HTLV-I). ATL carries a very bad prognosis because of intrinsic chemoresistance and severe immunosuppression. The viral transactivator protein Tax is responsible for several aspects of the malignant transformation such as proliferation, resistance to apoptosis, genetic instability, tumor dissemination, immnune escape and chemotherapy resistance. Through all of these activities, Tax acts as a powerful oncogene, and represents the most attractive viral protein for targeted therapy. Among Tax properties, activation of the NF-κB pathway plays a crucial role in the proliferation and transformation of the infected cells. Indeed, most of the activated cellular genes in HTLV-I infected cells are through this mechanism. Results. We have, using an in vitro model of ATL derived cells, identified several potential targeted therapies for ATL: 1) Arsenic trioxide (As) synergizes with interferon-α (IFN) to induce G1 arrest and apoptosis in ATL through shut-off of the NF-κB pathway and Tax degradation by the proteasome. This combination yielded promis- 112 | haematologica/the hematology journal | 2007; 92(s1) ing clinical results in relapsed/refractory ATL patients. 2) Clinically achievable concentrations of bortezomib, a selective proteasome inhibitor, targeted multiple cellular pathways that resulted in dramatic inhibition of cell proliferation and apoptosis of ATL-derived cells. 3) ATL cells secrete high concentrations of functional angiogenic factors, establish functional gap junctions with endothelial cells, and extravasate through the endothelial barrier using mechanisms involved in angiogenesis. Angiogenesis inhibitors, such as anti-VEGF monoclonal antibodies (bevasizumab) or specific kinase inhibitors of the VEGF receptors (PTK-787) inhibit ATL-induced angiogenesis and impede ATL cell invasion. We are investigating the in vivo therapeutic potential of these targeted therapies identified in our in vitro studies, using as a preclinical model SCID mice injected with lymphomatous spleen cells from transgenic mice for the Tax gene of HTLV-I. Results of these ongoing studies, with respect to tumor regression, apoptosis induction and survival will be presented. 0311 HE TYROSINE KINASE INHIBITOR DASATINIB SUPPRESSES IGE-DEPENDENT ACTIVATION AND HISTAMINE RELEASE IN BASOPHILS M. Kneidinger, 1 K. V. Gleixner, 1 A. Böhm, 1 A. Vales, 1 K. Sonneck, 1 S. Florian, 1 M. Weghofer, 1 C. Lupinek, 1 S. Vrtala, 1 R. Valenta, 1 G. Superti-Furga, 2 F.Y. Lee, 3 P. Valent1 1 Medical University of Vienna, VIENNA, Austria; 2 CeMM, Research Center f. Mol. Med., VIENNA, Austria; 3 Oncol. Drug Disc., Bristol-Myers Squibb, PRINCETON, NJ, USA Background. Dasatinib (BMS354825) is a small molecule-type inhibitory drug that blocks several tyrosine kinases including src kinases, PDGFR, KIT, and BCR/ABL. Recently, dasatinib has been introduced as a new effective antileukemic agent in patients with imatinib-resistant chronic myeloid leukemia (CML) and acute lymphocytic leukemia. Moreover, dasatinib may act on normal lymphocytes and other physiologic cells through diverse target structures. In particular, dasatinib has recently been examined for its immunosuppressive and anti-inflammatory effects. Methods and Results. We here report that dasatinib at 1 µM completely blocks the anti-IgE-induced release of histamine in human blood basophils in healthy subjects. The effects of dasatinib on histamine secretion in basophils were dose-dependent (IC50: 50-100 nM) and were found to be specific for IgE-dependent activation of basophils in that no inhibition was seen in C5a-activated or Ca-ionophore-exposed basophils. Moreover, dasatinib was found to block recombinant allergen-induced release of histamine from human basophils in sensitized individuals. In addition, as assessed by flow cytometry, dasatinib (1 µM) was found to inhibit the IgE-dependent upregulation of several activation-linked antigens, including aminopeptidase N (CD13), LAMP-3 (CD63), endolyn (CD164), and the basophil-related ecto-enzyme E- NPP3 (CD203c) on human basophils. The effects of dasatinib on upregulation of basophil differentiation antigens were found to be dosedependent and were seen in normal subjects as well as in allergic individuals. Conclusions. Dasatinib blocks IgE-mediated activation and histamine release in human blood basophils. These anti-allergic effects of dasatinib may have clinical implications and may point to additional indications for this multifunctional drug. 0312 MLN3897, A NOVEL CCR1 INHIBITOR, IMPAIRS OSTEOCLAST FORMATION AND FUNCTION ASSOCIATED WITH DOWNREGULATION OF C-FOS S. Vallet, 1 N. Raje,1 K. Ishitsuka, 1 T. Hideshima, 1 I. Breitktreutz, 1 T. Kiziltepe, 1 H. Yasui, 1 S. Pozzi, 1 D. Cirstea, 1 E. Ocio, 1 N. Shiraishi, 1 M. Ladetto, 2 M. Boccadoro, 2 K. Anderson1 1 2 Dana Farber Cancer Institute, BOSTON, USA; Università degli studi di Torino, TORINO, Italy Background. Osteolytic lesions due to enhanced osteoclast (OC) activity are a hallmark of myeloma bone disease and other metastatic cancers. Chemokines play a critical role in enhancing OC formation and activity. Aims.Since CCR1 is one of the main chemokine receptors expressed on monocytes and OC, we here characterized the effects of MLN3897 (Millennium Pharmaceuticals), a novel specific antagonist of CCR1, on OC formation and function. Methods. In order to analyze the effects of MLN3897 on osteoclastogenesis, we generated OC from peripheral blood mononuclear cells of healthy donors stimulated with RANKL and M-CSF (50 ng/mL) for 3 weeks, in the absence or presence of MLN3897. Mature OC were multinucleated TRAP+ cells, and their
functional activity was confirmed by pit formation and collagen release ELISA assays. Results. CCR1 expression was induced early during OC formation, at one week 60% of the monocyte population expressed CCR1 by flow cytometric analysis. Macrophage inflammatory protein- 1 α secretion was also stimulated, from 57 pg/mL at 24 hours to 156 pg/mL at one week. Treatment with MLN 3897 (10 nM) resulted in inhibition of both OC formation (by 40%) and function (by 70%) in a dosedependent way (p
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haematologica the hematology journa
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Information for readers, authors an
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EHA Executive Board E. Hellström-L
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Poster session I POSTER SESSION POS
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12 th Congress of the European Hema
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dasatinib. Methods. We studied Ikar
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Expression of the oncogene H-Ras an
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is the gene for the erythropoietin
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safety of a slow-release liposomal
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0029 OUTCOME OF THE TREATMENT OF AD
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drug-induced apoptotic response of
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41% in the PI3K- group (p=0.001). I
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Acute myeloid leukemia - Clinical I
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to 60 years (n=116, or 72%) receive
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0056 PROGNOSTIC SIGNIFICANCE OF FLT
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Anemia and Bone marrow failure 0061
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tified with the current protocol. S
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new cases of lead poisoning due to
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icance, from baseline to week 6 (p
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0086 THROMBELASTOGRAPHIC CHART RELI
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trials. The aim of this retrospecti
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tant function in this disease, nega
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ed to a favorable outcome. Bialleli
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stronger levels of p21 in the cell
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hematological centers in one countr
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ure 1). Conclusions. Results for re
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patients. After a median follow-up
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Cytogenetics and Molecular diagnost
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0135 ROUTINE DETECTION OF CYTOGENET
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(MMolR, defined as a BCR-ABL x 100
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0146 ARSENIC TRIOXIDE INDUCES ACCUM
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tinguish between genotypic B-cell l
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Genomics and proteomics 0158 PLASMA
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0164 EVALUATION OF MULTIPLEX LIGATI
Page 69 and 70: each patient’s replicate conditio
Page 71 and 72: 0174 RELATION BETWEEN LOW PML-RARα
Page 73 and 74: 0179 ESHAP VS GIN AS SALVAGE AND MO
Page 75 and 76: Immunology and gene therapy 0184 EA
Page 77 and 78: Cell viability was not affected by
Page 79 and 80: month is not relevant to chronic Gv
Page 81 and 82: Infection and supportive care I 020
Page 83 and 84: 0206 POTENTIAL ROLE OF CMV IN THE O
Page 85 and 86: 3H-thymidine uptake in cell culture
Page 87 and 88: 0217 TUBERCULOSIS AMONG A COHORT OF
Page 89 and 90: 0222 COMPARISON OF IWG 2006 AND IWG
Page 91 and 92: tem (IPSS) to h-MDS was also invest
Page 93 and 94: PCH97-19) were studied. Conventiona
Page 95 and 96: of erythroid colonies was reduced i
Page 97 and 98: 0245 POTENT AND SELECTIVE INHIBITIO
Page 99 and 100: 0250 INACTIVATION OF SUPPRESSOR OF
Page 101 and 102: Bortezomib 1.3 mg/m 2 days 1,4,8,11
Page 103 and 104: Response was defined according to E
Page 105 and 106: G-CSF can be used in neutropenic pa
Page 107 and 108: ence and functional activity of CD8
Page 109 and 110: itating tumor development, or engag
Page 111 and 112: phoma and SNT-13, -15 were establis
Page 113 and 114: usage (2/20 ie 10%) were observed.
Page 115 and 116: 0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
Page 117 and 118: (range, 1-6) and 11 treatment cycle
Page 119: 0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
Page 123 and 124: No major toxicity, neither hematolo
Page 125 and 126: enewal potential of X-RAR-positive
Page 127 and 128: (50-99) respectively. Serial analys
Page 129 and 130: cell-interaction, adhesion and acti
Page 131 and 132: 0340 ALTERED FIBRIN CLOT STRUCTURE
Page 133 and 134: Conclusions. This study demonstrate
Page 135 and 136: 0354 FACTOR V LEIDEN HOMOZYGOUS GEN
Page 137 and 138: Results. From July 2005 through Mar
Page 139 and 140: 0364 CLINICAL EFFICACY OF OXALIPLAT
Page 141 and 142: one marrow and peripheral blood ste
Page 143 and 144: ecently suggested (Boissel et al.,
Page 145 and 146: 0378 SAFETY AND EFFICACY OF THE TER
Page 147 and 148: Cytogenetics and molecular diagnost
Page 149 and 150: 0385 CYTOPLASMIC MUTATED NUCLEOPHOS
Page 151 and 152: 0390 ELTROMBOPAG RAISES PLATELET CO
Page 153 and 154: factor for the achievement of CR wa
Page 155 and 156: The cases of RAS showed two peaks o
Page 157 and 158: is 85%. Seven out of the 25 relapse
Page 159 and 160: 0409 FRACTIONATED RADIOIMMUNOTHERAP
Page 161 and 162: 0414 COMPARATIVE ANALYSIS OF THE CO
Page 163 and 164: successfully managed with GM-CSF di
Page 165 and 166: 49% for PCR positive patients (95%
Page 167 and 168: +8 (1 PR+1 HI) and 14/24 pts with c
Page 169 and 170: (e.g. bcr-abl leading to CML). CSC
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0438 TERC MUTATIONS ANALYSIS IN PAT
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observed in all mice. Analysis of l
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ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
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One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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genesis of acute myeloid leukaemia
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polymorphism at nucleotide 4889 of
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expression along with a decreased C
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0487 MUTATIONAL STATUS OF NUCLEOPHO
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previously reported, a single cours
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0497 SINGLE AGENT CLORETAZINE (VNP4
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ly received melphalan-based chemoth
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were similar among the 3 groups. Ho
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Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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0523 DNA REPAIR INHIBITION IN RESTO
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held true when BMI-1 expression was
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Ph + cells in the bone marrow). We
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derivative chromosome (4p16, 7p14,
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0545 STABILIZED BONE MARROW IS NOT
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obtained in low (Sokal) risk patien
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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patients had died of their underlyi
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scripts and proteins most affected
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modulated after 24 h (37 up- and 59
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0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
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Results. A total of 396 patients we
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C30 questionnaire, and the correspo
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wave length of light of reflected r
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0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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BRIC 126 and 4N1K) in cells lacking
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sclerosis[NS] and 12 Mixed cellular
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0927 MK-0457, A NOVEL MULTIKINASE I
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Publication Only 0933 CLINICAL FEAT
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HSCT from the available Asian as we
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that the incidence of JAK2 mutation
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without type 2 diabetes. Methods. T
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pts (38.8%) that were isolated (abs
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y using the Miltenyi CD34 isolation
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0969 COMPARISON OF CD25 IMMUNOHISTO
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cytes was 24 days (range 8-32 days)
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a cytogenetic hallmark for M4/M5 su
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normal human BM B progenitor cells
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0994 INCIDENCE OF INVASIVE ASPERGIL
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3 of disease relapse.TRM at day+100
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survival of five years. This dismal
Page 383 and 384:
1011 FLOW CYTOMETRIC DNA INDEX AND
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1018 THE EFFECT OF THE SUGARBAKER P
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1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
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1063 ABNORMAL METHYLATION STATUS OF
Page 403 and 404:
1069 CLINICAL RELEVANCE OF REGULATO
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1076 SERUM LEVELS OF SOLUBLE HLA CL
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patient is still undergoing intensi
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nificant MVD differences were detec
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dictor of OS (p=0.004). High dose t
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1099 ALTERATIONS IN THE NATURAL KIL
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1105 CYTOGENETIC ABNORMALITIES IN 3
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1110 CONSTITUTIVE ACTIVATION OF STA
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efficacy results with a well-tolera
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unmutated VH genes, and high and lo
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Aims. Aim of this study was to pred
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tested across a wide range of human
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were incidentally diagnosed (52%).
Page 429 and 430:
ß2GP1 may be considered as determi
Page 431 and 432:
characterized in 198 β thalassaemi
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
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of the drug is crucial to allow lon
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egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
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events -Postoperative states: 9,19%
Page 451 and 452:
efficacy and decreased atherosclero
Page 453 and 454:
1217 INCIDENCE OF EARLY STAGE IDIOP
Page 455 and 456:
1691GA and 1 homozygous 1691AA. The
Page 457 and 458:
1230 ASSOCIATION OF HEPARANASE GENE
Page 459 and 460:
posed, was: DF = (CD43%+FMC7%+CD79b
Page 461 and 462:
treatment of acute promyelocityc le
Page 463 and 464:
loaded group and 35 (70%) were non-
Page 465 and 466:
mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
Page 469 and 470:
ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
Page 475 and 476:
disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
Page 479 and 480:
phamide 750 mg/m 2 on day 1, vincri
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
Page 497 and 498:
Results. Though there was no recogn
Page 499 and 500:
2% and 19% of patients with or with
Page 501 and 502:
were older than 65 y) which can be
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
Page 505 and 506:
median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
Page 509 and 510:
to the presence of IVS1-6 mutation
Page 511 and 512:
fy predictive factors for these abn
Page 513 and 514:
acute leukemia. However, we cannot
Page 515 and 516:
agents. They involve primarily the
Page 517 and 518:
voriconazole for 2 months followed
Page 519 and 520:
typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
Page 523 and 524:
with development of BC/AP. 2. EVI-1
Page 525 and 526:
1447 THE IMPACT OF DISPARITY IN SHO
Page 527 and 528:
three had visual field defects, two
Page 529 and 530:
acquired mutation most prone to cau
Page 531 and 532:
1466 ROS GENERATION AND APOPTOSIS I
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1473 DIARRHEIC SYNDROME, A CLINICAL
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gene fusion is an independent progn
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1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
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immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
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Hodgkin’s disease is well known,
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gram provided a unique chance to de
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even when ADP-induced plt activatio
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medullary involvement of multiple m
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
Page 559 and 560:
Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
Page 567 and 568:
El-Sharkawy, N., 0016 Elwahidi, G.,
Page 569 and 570:
Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
Page 573 and 574:
Jaksic, B., 0127, 0446 Jaksic, O.,
Page 575 and 576:
Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
Page 581 and 582:
Musto, P., 0254, 0401, 0422, 0569,
Page 583 and 584:
Papadavid, E., 1442 Papageorgiou, E
Page 585 and 586:
Probatova, N., 0704 Prochazka, V.,
Page 587 and 588:
Rykavicin, O., 0504 Ryningen, A., 0
Page 589 and 590:
Sirard, C., 0127, 0128 Sirigou, A.,
Page 591 and 592:
Thiebaut, A., 0454 Thieblemont, C.,
Page 593 and 594:
Vincenzi, C., 1060 Viniou, N.-A., 0
Page 595 and 596:
Zouabi, H., 0503, 0999 Zoumbos, N.C
Page 597 and 598:
Page 599 and 600:
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Page 603:
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12th Congress of the European Hematology ... - Haematologica

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