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12 th Congress of the European Hematology Association trimethoprim/sulfamethoxazole DS and famciclovir treatment during therapy and until CD4 + counts were ≥200 cells/µL. The primary endpoint was PFS; secondary endpoints included response rate, time to alternative therapy, survival, and safety. A total of 297 patients were randomized (CAM n=149 and CHLO n=148; median age: 60 years); performance status 0-1: 96%; maximum lymph node size ≥5 cm: 22%; and Rai stage I-II: 63%. An independent response review panel (IRRP) confirmed diagnosis, Rai stage, response and disease progression that were used in the efficacy analysis. Results. PFS was superior for CAM (p=0.0001, stratified log-rank test) with a hazard ratio of 0.58 (95%CI: 0.43, 0.77). Response rate was higher for CAM than CHLO, previously reported (ASH, 2006;301). CAM was superior to CHLO in patients
Cytogenetics and Molecular diagnostics I 0129 PARENTAL ORIGIN DETERMINATION I FISH A NEW METHOD TO CHARACTERIZE THE PARENTAL ORIGIN OF HUMAN CHROMOSOMES ON A SINGLE CELL LEVEL M. Gross, 1 H. Mkrtchyan, 2 H. Thieme, 1 F. Von Eggeling, 1 B. Horsthemke, 1 Chr. Jonsrud, 3 U. Claussen, 1 TH Liehr, 1 A. Weise1 1 Institute of Human Genetics, JENA, Germany; 2 Yerevan State University, YEREVAN, Armenia; 3 Dept. of Medical Genetics, TROMSO, Norway The discrimination of homologues (chromosomal) regions could up to now be done exclusively by molecular genetic Aims.using microsatellite or SNP-analysis. Only in exceptional cases a distinction on a single cell level by chromosomes was possible. Therefore, we developed a method called parental origin determination fluorescence in situ hybridization (pod-FISH) that is suited for a single cell analysis and can distinguish every homologues chromosome pair on the basis of copy number polymorphisms (CNP). Presently we selected 225 of over 2191 reported polymorphic regions in the human genome and used them as pod-FISH probes. pod-FISH results were verified by microsatellite analysis. We established pod-FISH probe sets for all 24 human chromosomes. To enable working with more than one polymorphic BAC probe at the same time, chromosome specific pod-FISH sets using 5 different fluorochromes were developed. For larger chromosomes like chromosomes 1, 2, 3, 4, 6, 9 and X it was more convenient to create chromosome arm specific pod-FISH sets for an easier analysis and to prevent double labeling. Up to now two cases with a known UPD, 2 cases with maternal contamination and three leukemia cases (AML with trisomy 8) were analyzed successfully. Also the method was applied on a unique case which is a chimera of two cell lines: one female cell line with a complete paternal isodisomy (97%) and one normal male cell line (3%). The results obtained by pod-FISH were in complete concordance with data obtained by microsatellite-analysis. The usefulness and feasibility of the new pod- FISH approach was compared to conventional microsatellite analysis and proved to be as reliable. Thus, the pod-FISH method will open new horizons for diagnostic and scientific fields that could not be questioned by now. E.g. the analysis of single cells will allow in leukaemia to get new diagnostic markers for therapy control after transplantations or to detect maternal contamination in prenatal diagnosis. Supported in parts by a grant from the university of Jena, the Deutsche Krebshilfe (70-3125-Li1), the INTAS (AISbl 03-51-4060), the IZKF Jena (Start-up S16), the DFG (436 ARM 17/5/06, LI 820/9-1), the IZKF together with the TMWFK (TP 3.7 and B307-04004), Stiftung Leukämie and the Ernst-Abbe- Stiftung. 0130 ALTERATIONS OF THE TP53 IN AML AND CLL ARE STRONGLY ASSOCIATED WITH A COMPLEX ABERRANT KARYOTYPE C. Haferlach, F. Dicker, H. Herholz, S. Schnittger, W. Kern, T. Haferlach MLL - Munich Leukemia Laboratory, MUNICH, Germany The TP53 gene is the most frequently mutated gene in human tumors identified so far. However, in leukemia TP53 alterations seem to be rare. It was the aim of this study to determine the incidence of TP53 mutations in AML and CLL and analyze their relation to cytogenetic and other molecular genetic aberrations. Overall 235 AML cases were analyzed for TP53mutations, FLT3-length mutations (FLT3-LM), MLL partial tandem duplication (MLL-PTD) and NPM1 mutations. TP53 mutation screening of exons 3-9 was performed by denaturing high performance liquid chromatography (DHPLC). All mutations detected were verified by direct sequencing. The first 149 patients were unselected, the remaining were selected to increase the numbers in rare cytogenetic subgroups. In the unselected cohort a TP53 mutation was detected in 13.4% (20/149 cases). In the total cohort a TP53 mutation was observed in 33 of 235 cases (14%). 29 of these 33 cases (87.9%) showed a complex aberrant karyotype. In the four remaining cases with TP53 mutation a normal karyotype, a trisomy 8, a trisomy 13, and a t(8;21)(q22;q22) each as the sole abnormality were observed, respectively. This data confirms results from our previous independent series demonstrating a high incidence of TP53 mutations in AML with complex aberrant karyotype (1. series 78%, current series 69%). In all other cytogenetic subgroups TP53 mutations are very rare (4/193, 2.1%). Two cases withTP53 mutation showed also a FLT3-LM and one a MLL-PTD. TP53-mutations were not found together with NPM1 muta- 12 th Congress of the European Hematology Association tions. In addition 194 consecutive CLL patients were screened for TP53deletion by fluorescence in situ hybridization (FISH) and for TP53-mutations. A TP53 deletion was detected by FISH in 18 cases (9.3%). 16 of these 18 cases also showed a TP53 mutation. In four further cases without a TP53 deletion a TP53 mutation was observed. Therefore, the total incidence of TP53 alterations in CLL was 11.3% (22/194) with a significant association between TP53 deletions and TP53 mutations (p
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haematologica the hematology journa
Page 3 and 4: Information for readers, authors an
Page 5 and 6: EHA Executive Board E. Hellström-L
Page 7 and 8: Poster session I POSTER SESSION POS
Page 9 and 10: 12 th Congress of the European Hema
Page 11 and 12: dasatinib. Methods. We studied Ikar
Page 13 and 14: Expression of the oncogene H-Ras an
Page 15 and 16: is the gene for the erythropoietin
Page 17 and 18: safety of a slow-release liposomal
Page 19 and 20: 0029 OUTCOME OF THE TREATMENT OF AD
Page 21 and 22: drug-induced apoptotic response of
Page 23 and 24: 41% in the PI3K- group (p=0.001). I
Page 25 and 26: Acute myeloid leukemia - Clinical I
Page 27 and 28: to 60 years (n=116, or 72%) receive
Page 29 and 30: 0056 PROGNOSTIC SIGNIFICANCE OF FLT
Page 31 and 32: Anemia and Bone marrow failure 0061
Page 33 and 34: tified with the current protocol. S
Page 35 and 36: new cases of lead poisoning due to
Page 37 and 38: icance, from baseline to week 6 (p
Page 39 and 40: 0086 THROMBELASTOGRAPHIC CHART RELI
Page 41 and 42: trials. The aim of this retrospecti
Page 43 and 44: tant function in this disease, nega
Page 45 and 46: ed to a favorable outcome. Bialleli
Page 47 and 48: stronger levels of p21 in the cell
Page 49 and 50: hematological centers in one countr
Page 51 and 52: ure 1). Conclusions. Results for re
Page 53: patients. After a median follow-up
Page 57 and 58: 0135 ROUTINE DETECTION OF CYTOGENET
Page 59 and 60: (MMolR, defined as a BCR-ABL x 100
Page 61 and 62: 0146 ARSENIC TRIOXIDE INDUCES ACCUM
Page 63 and 64: tinguish between genotypic B-cell l
Page 65 and 66: Genomics and proteomics 0158 PLASMA
Page 67 and 68: 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
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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
Page 257 and 258:
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
Page 331 and 332:
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
Page 337 and 338:
0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
Page 341 and 342:
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
Page 347 and 348:
2004 to January, 2006. At enrollmen
Page 349 and 350:
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
Page 365 and 366:
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
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
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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
Page 401 and 402:
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
Page 409 and 410:
nificant MVD differences were detec
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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
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were incidentally diagnosed (52%).
Page 429 and 430:
ß2GP1 may be considered as determi
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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
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
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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
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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
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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
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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.
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ly. Conclusions. 1. Combined intens
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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
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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
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1466 ROS GENERATION AND APOPTOSIS I
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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
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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,
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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.,
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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:
12 th Congress of the European Hema
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