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12 th Congress of the European Hematology Association AMLMD/tAML 27, MDS/tMDS 18) who received 71 FLA cycles, (10 FLA, 61 FLA+Ida) in which unconjugated filgrastim (dosage: 300 mcg/sqm/day) was given from day 12 until neutrophils recovery (>500/mmc); status before chemo: untreated 41 (57.7%), CR/PR 14 (19.7%), active disease 16 (22.6%). Hematological recovery was evaluated only in pts with a documented response to treatment (complete remission, CR, or partial remission, PR). Median values of CTC grade 4 neutropenia and thrombocytopenia duration in the two groups were compared with the Mann Whitney U-test; cases of documented infections and episodes of fever of unknown origin (FUO) were reported and incidence in the two groups was compared with the chi-square test. Table 1. Results. full results are shown in the Table 1; in one case a second PEGfilgrastim injection was administered at day 32 for delayed recovery. Conclusions. our preliminary results suggest that a single PEG-filgrastim injection after FLA regimens is equivalent to daily unconjugated filgastrim; in fact, haematological recovery and incidence of infective/FUO episodes during grade 4 neutropenia resulted comparable in the two groups of pts. Confirmation in a larger population of pts is warranted. Moreover, as the single dose is preferred by pts to daily injections, the overall costeffectiveness of the PEG-filgrastim formulation could prove favourable. 1086 HYPEREOSINOPHILIC SYNDROMES (HESS)-CLINICAL PRESENTATION AND VARIABLE RESPONSE TO TREATMENT-A CASE SERIES S. Mitra, 1 P. Thornton, 2 P.T. Murphy3 1 Mater University Hospital, DUBLIN; 2 Connolly Hospital,Dublin 15, DUBLIN, Ireland; 3 Beaumont Hospital, DUBLIN, Ireland Background. Hypereosinophilic syndromes (HESs) refers to a heterogenous group of disorders characterised by marked blood eosinophilia (>1500/cu mm) and tissue eosinophilia (lasting for more than 6 months),in the absence of other eitiologies for eosinophilia, resulting in end organ damage. Eosinophilias may be a reactive condition or due to a chronic myeloproliferative disorder( with evidence of clonal proliferation).Reactive eosinophilias are due to release of cytokines(IL-3,IL- 5,GM-CSF etc) and the common causes are parasitic infections, allergic diseases, vasculitides, drug reactions and malignancies .Clonal eosinophilias are those in which the eosinophilia is a part of a clonal haematological malignancy, which is very often associated with the fusion gene FIP1L1-PDGFR α which causes the generation of a constitutively active Tyrosine Kinase.Several visceral complications like cardiomyopathies, nervous system involvement (eg paraparesis, cerebral infarction, eosinophilic meningitis etc) are often fatal illnesses. Treatment modalities for HES includes corticosteroids, chemotherapeutic agents (hydroxyurea cyclophosphamide , vincristine) and α-interferon. Newer treatment modalities including tyrosine kinase inhibitors (eg Imatinib mesylate) and monoclonal anti-IL5 antibodies are now available. Patients carrying this fusion gene respond well to the Tyrosine Kinase Inhibitor,Imatinib. Some patients with HES,that are negative for this fusion gene may also respond to Imatinib, suggesting that in such cases other Tyrosine Kinases may be dysregulated. Aims. Retrospective review of the variable response of 7 patients with HES (over a period of 6 months),to current treatment modalities. Methods.The 7 patients (6 Male, 1 Female; age range 37-80 yrs; mean age 56 yr) presented with eosinophilia in the range 2600-73,000 /cu mm. A response to treatment was defined as Eosinophil count80 yr) was treated with Hydroxyurea initially. Table 1. HES-Patient Characteristics. Results. Four of the six patients receiving Imatinib responded to it. Of the 2 patients not responding to Imatinib,1 responded par- tially to Hydroxyurea and the other did not respond to monotherapy with steroid or α-interferon (but eventually responded to a combination of the two). The patient who had initial treatment with Hydroxyurea responded well. Of the 7 patients 1 was positive for the FIP1L1-PDGFRa fusion gene,1 result was equivocal, 3 were negative and 2 were not tested. Of the 2 that were negative 1 responded to Imatinib. Conclusions. Thus response of HES patients to the various treatment modalities, is variable and often unpredictable. A trial of Imatinib is worthwhile in all cases,including the FIP1 negative cases. 1087 CHOICE OF ENDOTHELIAL MARKER IS CRUCIAL FOR QUANTIFICATION OF BONE MARROW MICROVESSEL DENSITY IN CHRONIC LYMPHOCYTIC LEUKEMIA L. Smolej, P. Kasparova, D. Belada, P. Zak University Hospital and Medical School, HRADEC KRALOVE, Czech Republic Introduction. Angiogenesis is a potential prognostic factor in chronic lymphocytic leukemia (CLL). Elevated levels of angiogenic factors have been found in peripheral blood of CLL patients. However, results of studies assessing bone marrow neovascularization in CLL are controversial, in part due to different antibodies used for immunohistochemical identification of endothelial cells and different methods of assessing microvessel density (MVD). Moreover, there are insufficient data regarding relationship of marrow angiogenesis to prognostic markers in CLL such as clinical stage, pattern of marrow infiltration, genetic abnormalities detected by FISH, or mutation status of immunoglobulin heavychain variable-region genes (IgVH). Aims. 1. To quantify MVD in bone marrow biopsies from CLL patients and control group using two different monoclonal antibodies and reproducible method of vessel counting; 2. To assess relationship of MVD to most important prognostic factors. Methods. We analyzed MVD in bone marrow biopsies from untreated patients with CLL using immunohistochemical staining of endothelial cells with monoclonal antibodies against CD34 (n=22) and von Willebrand factor (vWF, n=18). Control group consisted of 17 biopsies from age- and sex-matched individuals without evidence of malignancy in bone marrow. Microvessel density was assessed under light microscope equipped with image analysis software and calculated using hot spot method, i.e. identification of three loci with highest accumulation of microvessels under low (100x) magnification and counting microvessels in three high-power fields (400x) per hot spot. MVD was expressed as mean number of microvessels per mm2 . CLL cohort was further subdivided according to clinical course (stable vs. progressive), Rai stage (0 vs. I-IV), pattern of marrow infiltration (non-diffuse vs. diffuse), genetic abnormalities (favourable, i.e. no abnormality or del13q14 as a sole aberration vs. unfavourable, i.e. del 17p / del11q / +12), and IgVH mutation status (mutated vs. unmutated). Results. MVD was significantly elevated in CLL group in comparison to controls using either antibody (CD34, mean±standard deviation [SD], 75.6±50.6, 95% confidence interval of mean [CI], 53.2-98.1 vessels/mm2 vs. 47.4±21.8, 95% CI, 36.2-58.6 vessels/mm2 , p=0.039; vWF, 21.3±16.5 vessels/mm2 , 95% CI, 13.1-29.5 vs. 11.5±8.5, 95% CI, 6.8-16.2 vessels/mm2 , p=0.017). However, no sig-
nificant MVD differences were detected between CLL subgroups with regard to clinical course, pattern of marrow infiltration, Rai stage, FISH abnormalities or IgVH mutation status. Interestingly, there was a significant difference between MVD counts according to antibody used: MVD was higher using CD34 vs.vWF in CLL as well as control group (p60 years (2022.65 per 100000/year; 95% CI 813.2-4167.5 per 100000/year) than in MGUS patients
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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
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each patient’s replicate conditio
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0174 RELATION BETWEEN LOW PML-RARα
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0179 ESHAP VS GIN AS SALVAGE AND MO
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Immunology and gene therapy 0184 EA
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Cell viability was not affected by
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month is not relevant to chronic Gv
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Infection and supportive care I 020
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0206 POTENTIAL ROLE OF CMV IN THE O
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3H-thymidine uptake in cell culture
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0217 TUBERCULOSIS AMONG A COHORT OF
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0222 COMPARISON OF IWG 2006 AND IWG
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tem (IPSS) to h-MDS was also invest
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PCH97-19) were studied. Conventiona
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of erythroid colonies was reduced i
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0245 POTENT AND SELECTIVE INHIBITIO
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0250 INACTIVATION OF SUPPRESSOR OF
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Bortezomib 1.3 mg/m 2 days 1,4,8,11
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Response was defined according to E
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G-CSF can be used in neutropenic pa
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ence and functional activity of CD8
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itating tumor development, or engag
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phoma and SNT-13, -15 were establis
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usage (2/20 ie 10%) were observed.
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0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
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(range, 1-6) and 11 treatment cycle
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0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
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functional activity was confirmed b
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No major toxicity, neither hematolo
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enewal potential of X-RAR-positive
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(50-99) respectively. Serial analys
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cell-interaction, adhesion and acti
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0340 ALTERED FIBRIN CLOT STRUCTURE
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Conclusions. This study demonstrate
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0354 FACTOR V LEIDEN HOMOZYGOUS GEN
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Results. From July 2005 through Mar
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0364 CLINICAL EFFICACY OF OXALIPLAT
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one marrow and peripheral blood ste
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ecently suggested (Boissel et al.,
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0378 SAFETY AND EFFICACY OF THE TER
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Cytogenetics and molecular diagnost
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0385 CYTOPLASMIC MUTATED NUCLEOPHOS
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0390 ELTROMBOPAG RAISES PLATELET CO
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factor for the achievement of CR wa
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The cases of RAS showed two peaks o
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is 85%. Seven out of the 25 relapse
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0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
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successfully managed with GM-CSF di
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49% for PCR positive patients (95%
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+8 (1 PR+1 HI) and 14/24 pts with c
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(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
Page 357 and 358: Publication Only 0933 CLINICAL FEAT
Page 359 and 360: HSCT from the available Asian as we
Page 361 and 362: that the incidence of JAK2 mutation
Page 363 and 364: without type 2 diabetes. Methods. T
Page 365 and 366: pts (38.8%) that were isolated (abs
Page 367 and 368: y using the Miltenyi CD34 isolation
Page 369 and 370: 0969 COMPARISON OF CD25 IMMUNOHISTO
Page 371 and 372: cytes was 24 days (range 8-32 days)
Page 373 and 374: a cytogenetic hallmark for M4/M5 su
Page 375 and 376: normal human BM B progenitor cells
Page 377 and 378: 0994 INCIDENCE OF INVASIVE ASPERGIL
Page 379 and 380: 3 of disease relapse.TRM at day+100
Page 381 and 382: survival of five years. This dismal
Page 383 and 384: 1011 FLOW CYTOMETRIC DNA INDEX AND
Page 385 and 386: 1018 THE EFFECT OF THE SUGARBAKER P
Page 387 and 388: 1024 KIR/HLA CLASS I MISMATCHING AN
Page 389 and 390: ment details and thrombotic histori
Page 391 and 392: 1036 INCIDENCE AND SPECTRUM OF INFE
Page 393 and 394: tinely by our stem cell lab prior t
Page 395 and 396: tion to a translocation t(5;14)(q35
Page 397 and 398: ment of CML and induces a high rate
Page 399 and 400: due to reactivation and/or progress
Page 401 and 402: 1063 ABNORMAL METHYLATION STATUS OF
Page 403 and 404: 1069 CLINICAL RELEVANCE OF REGULATO
Page 405 and 406: 1076 SERUM LEVELS OF SOLUBLE HLA CL
Page 407: patient is still undergoing intensi
Page 411 and 412: dictor of OS (p=0.004). High dose t
Page 413 and 414: 1099 ALTERATIONS IN THE NATURAL KIL
Page 415 and 416: 1105 CYTOGENETIC ABNORMALITIES IN 3
Page 417 and 418: 1110 CONSTITUTIVE ACTIVATION OF STA
Page 419 and 420: efficacy results with a well-tolera
Page 421 and 422: unmutated VH genes, and high and lo
Page 423 and 424: Aims. Aim of this study was to pred
Page 425 and 426: tested across a wide range of human
Page 427 and 428: 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
Page 435 and 436: to-pelvic or perineal trauma. No me
Page 437 and 438: in age. High prevalence of LBM amon
Page 439 and 440: ecause some of the patients were or
Page 441 and 442: of the drug is crucial to allow lon
Page 443 and 444: egarding cost analysis of ASCT in G
Page 445 and 446: ID Allo-BMT, 1 family one mismatche
Page 447 and 448: admitted to ICU were discharged des
Page 449 and 450: 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
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posed, was: DF = (CD43%+FMC7%+CD79b
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treatment of acute promyelocityc le
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loaded group and 35 (70%) were non-
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mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
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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
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oped mild thrombocytopenia (platele
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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
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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
Page 533 and 534:
1473 DIARRHEIC SYNDROME, A CLINICAL
Page 535 and 536:
gene fusion is an independent progn
Page 537 and 538:
1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
Page 541 and 542:
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
Page 549 and 550:
even when ADP-induced plt activatio
Page 551 and 552:
medullary involvement of multiple m
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
Page 555 and 556:
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:
Page 601 and 602:
Page 603:
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