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12 th Congress of the European Hematology Association Myelodysplastic syndromes 0426 CYTOGENETIC HYBRIDIZATION BY ARRAY COMPARATIVE GENOMIC HYBRIDIZATION AND FLUORESCENCE IN SITU HIBRIDIZATION OF MESENCHYMAL STEM CELLS FROM PATIENTS WITH MYELODYSPLASTIC SYNDROMES O. López Villar, 1 F. Martín Sánchez-Guijo, 1 J.L. García, 2 E. Villarón, 1 N. López-Holgado, 1 J.A. Pérez Simón, 1 J. San Miguel, 1 M.C. Cañizo1 1 Hospital Universitario de Salamanca, SALAMANCA; 2 Centro de Investigación del Cancer, SALAMANCA, Spain Background. Myelodysplastic syndromes (MDS) are a group of clonal disorders of hematopoietic stem cell (HSC). The hematopoietic microenvironment plays a role in the physiology of the hematopoietic system, and mesenchymal stem cells (MSC) are a key component of this microenviroment. Recently, some data has been published showing that these MSC could be involved in the MDS pathophysiology. Moreover, the presence of cytogenetic aberrations on these cells is controversial. The studies performed, so far, have used conventional cytogenetics and fluorescent in situ hybridization (FISH). Aims. To characterize bone marrow derived MSC from patients with MDS, by two approaches: array comparative genomic hybridization (array-CGH), and FISH, in order to know genomic changes in these cells and whether they could show clonal cytogenetic alterations. Methods. 13 patients with untreated MDS were included in the study. The median age was 72 years (range: 54-89) The male/female ratio was 7/6. Diagnosis of MDS was established according to the WHO classification as follows: 5q- syndrome (n=7), refractory anemia (RA) (n=2), refractory anemia with ringed sideroblasts (RARS) (n=1) and refractory anemia with excess blasts type II (RAEB-II) (n=3). Standard cytogenetic and FISH studies on hematopoietic cells were performed at diagnosis according to standard methods with the following Results. 5q- (n=7), 8 trisomy (n=2) and normal cytogenetics (n=4). MSC were obtained by plating mononuclear cells from BM and cultured in a DMEM + 10% fetal calf serum medium, and expanded following standard procedures, until the third passage, when adherent MSC were harvested to perform cytogenetic and phenotypical studies. Array-CGH was performed in 11 cases and FISH studies in 5 (3 cases had both techniques). To perform Array-CGH a total of 3500 genomic targets were compounded from RP-11 libraries. The PCR products after purification were arrayed onto glass slides using a BioRobot. DNA was labelled, denaturalised and hybridizated. Images were analysed by using GenePix Pro 4.0 software. Results. MSC showed characteristic phenotypical data and their purity was 91%. In all cases analysed MSC showed DNA genomic changes. The most frequent aberrations were 1q24q32 region gains, in 72% of the cases, and 1p13 and 11q12 losses in 55% of patients. When the cells from patients carrying the 5q- alteration were analysed we observed that in half of them 5q losses were present in MSC. FISH analysis was carried out in MSC from 3 patients with 5q- and 2 patients diagnosed of RARS and RAEB-II, who had trisomy 8, and the same changes were present in 11% of MSC. Conclusions. We conclude that 100% of MSC from MDS show chromosomal aberrations when CGH arrays are used for this analysis. Even clonal specific MDS alterations are also shown when both, FISH and array-CGH analysis are performed. This is the first study that has showed the gains and losses in DNA of MSC from MDS by Array-CGH. MSC aberrations were also confirmed by FISH. 0427 HAS TREATMENT WITH EPO+/- G-CSF AN IMPACT ON PROGRESSION TO AML AND SURVIVAL IN LOW/INT-1-RISK MDS? A COMPARISON BETWEEN FRENCH-EPO PATIENTS AND THE IMRAW DATABASE S. Park, 1 S. Grabar, 1 C. Kelaidi, 2 O. Beyne-Rauzy, 3 F. Picard, 1 D. Vassilieff, 1 V. Coiteux,4 G. Leroux, 4 P. Leppeley, 4 H. Dombret, 4 M.T. Daniel, 4 S. Cheze, 4 B. Mahe, 4 L. Ades, 2 A. Ferrant, 4 C. Ravoet, 4 N. Vey, 4 M. Escoffre-Barbe, 4 L. Aljassem, 4 K. Bourgeois, 5 P. Greenberg, 6 P. Fenaux, 2 F. Dreyfus1 1 Cochin Hospital, PARIS, France; 2 Hôpital Avicenne, BOBIGNY, France; 3 Hôpital de Purpan, TOULOUSE, France; 4 GFM, PARIS, France; 5 University of Rochester Medical Center, NEW YORK, USA; 6 Stanford University Cancer Center, STANFORD, USA Backround. We recently reported the results of treatment with EPO ±G-CSF in 419 patients (Park, ASH 2006, n°522) treated between 1998 158 | haematologica/the hematology journal | 2007; 92(s1) and 2005 in France. Aims. Here we compared the outcome (progression to AML and survival) of these French patients (French-EPO) to MDS patients who received only supportive care (IPSS/IMRAW database). Methods. We restricted the analysis to patients with low and int-1 IPSS and also excluded CMML, RAEB-t, unclassifiable MDS, poor- risk karyotype, and 3q26 deletion, that are classically not the best candidates for EPO treatment. Progression to death and progression to AML since MDS diagnosis were compared using Kaplan-Meier estimates and Log-rank test. Multivariate cox analyses were adjusted for the main known prognostic factors (age at diagnosis, sex,% of marrow blasts, FAB diagnosis, IPSS score and karyotype). EPO introduction was modeled as a timedependent covariate (dependent on the delay between MDS diagnosis and EPO introduction). Results. In the French-EPO (F), 284 pts, and in the IMRAW database (I), 447 pts were finally compared. Median follow-up was 26 months (IQR 13-53) and 33 months (IQR 15-61) in French-EPO and IMRAW, respectively. Both cohorts were different for: age (median 71 vs 68 y, p=0.0013),% of blasts (median, 3% [IQR 2-5] vs 2% [IQR 1- 4], p=0.0006), FAB diagnosis [RA= 39% vs 56%, RAEB= 22% vs 17%, and RARS=38% vs 26%, (p
+8 (1 PR+1 HI) and 14/24 pts with complex karyotype (3 CR+9 PR+2 HI). OR was 59%, 65% and 75% for IPSS high (p=NS), int-2 (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
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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.
Page 115 and 116: 0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
Page 117 and 118: (range, 1-6) and 11 treatment cycle
Page 119 and 120: 0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
Page 121 and 122: functional activity was confirmed b
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: 49% for PCR positive patients (95%
Page 169 and 170: (e.g. bcr-abl leading to CML). CSC
Page 171 and 172: 0438 TERC MUTATIONS ANALYSIS IN PAT
Page 173 and 174: observed in all mice. Analysis of l
Page 175 and 176: ex-vivo expansion of HUCB-derived H
Page 177 and 178: ic kidney disease in univariate or
Page 179 and 180: One hundred eleven CN AML patients,
Page 181 and 182: to asses intestinal epithelial dama
Page 183 and 184: genesis of acute myeloid leukaemia
Page 185 and 186: polymorphism at nucleotide 4889 of
Page 187 and 188: expression along with a decreased C
Page 189 and 190: 0487 MUTATIONAL STATUS OF NUCLEOPHO
Page 191 and 192: previously reported, a single cours
Page 193 and 194: 0497 SINGLE AGENT CLORETAZINE (VNP4
Page 195 and 196: ly received melphalan-based chemoth
Page 197 and 198: were similar among the 3 groups. Ho
Page 199 and 200: Methods. Several read-out systems w
Page 201 and 202: 0518 SERUM AND CELLULAR EXPRESSION
Page 203 and 204: 0523 DNA REPAIR INHIBITION IN RESTO
Page 205 and 206: held true when BMI-1 expression was
Page 207 and 208: Ph + cells in the bone marrow). We
Page 209 and 210: derivative chromosome (4p16, 7p14,
Page 211 and 212: 0545 STABILIZED BONE MARROW IS NOT
Page 213 and 214: obtained in low (Sokal) risk patien
Page 215 and 216: 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
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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
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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%).
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ß2GP1 may be considered as determi
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characterized in 198 β thalassaemi
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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
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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%
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efficacy and decreased atherosclero
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1217 INCIDENCE OF EARLY STAGE IDIOP
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1691GA and 1 homozygous 1691AA. The
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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
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1265 POSACONAZOLE THERAPY IN REFRAC
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ly express the cytoplasmic (inactiv
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findings confirmed the significant
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a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
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phamide 750 mg/m 2 on day 1, vincri
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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
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(range 1-7) and 28,6% of patients h
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three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
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Results. Though there was no recogn
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2% and 19% of patients with or with
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were older than 65 y) which can be
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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
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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
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agents. They involve primarily the
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voriconazole for 2 months followed
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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
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three had visual field defects, two
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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
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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
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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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