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12 th Congress of the European Hematology Association every 30 minutes. The rats were randomly allocated to one of 3 arms: Replacement of blood volume with an equal volume of physiologic saline, replacement of blood volume with an equal volume of AQIX ® RS- I (Res-Del International Ltd., London, UK) or no replacement of blood losses. The primary end point of the study was the death of the animal documented by cardio-respiratory arrest. Results. Rats in the no-resuscitation arm had the shortest survival and least blood volume withdrawn. Survival time and mean volume withdrawn were significantly improved by the addition of either normal saline or AQIX ® RS-I resuscitation. AQIX ® RS-I provided a statistically superior survival time (p
survival of five years. This dismal prognosis is mostly due to resistance of MM to conventional therapies. Therefore, some of the attention has been redirected toward studying the role of bone marrow microenvironment in MM progression in order to find new ways to inhibit tumor growth by blocking interaction between tumor cells and their microenvironment. The important role of endothelium, osteoclasts and osteoblasts in MM progression has been documented. Aims. In this study we assessed the influence of myeloma-derived microvesicles (MMV) on human mesenchymal stem cells (MSC) by stimulating them with MMV. We compared also the gene expression profile in bone marrow stromal cells (MSC) from four healthy subjects (hMSC) and from six MM patients (mMSC). Methods. MMV were isolated from MM cell lines supernatants. Expression level of mRNA for genes involved in angiogenesis, invasion and MSC proliferation and osteoblastic differentiation were evaluated using real-time RT-PCR. Results. hMSC were exposed to 30 mg/mL of MMV for 8 and 24 hours and changes in gene expression were quantified. We noticed increased level of IL8 expression: 4.5 fold after 8 hours and 2 fold after 24 hours stimulation. Upregulation of MMP9 level was seen at 8 and 24 hours. HGF expression was decreased by approximately 2 folds at both 8 and 24 hours. 8 - hour exposure to MMV resulted in downregulation of RUNX2, collagen1 and osteocalcin mRNA by 1.5, 3 and 2 folds, respectively. After 24 hours, level of RUNX2 and collagen1 remained constant and level of osteocalcin decreased to 3.5 folds. When we analyzed gene expression in mMSC in comparison to hMSC we observed increased level of IL8 by 14 folds, VEGF and MMP9 by 3 folds, and decreased level of HGF by 2 folds. Difference in osteogenic genes expression in mMSC were also observed. RUNX2, collagen1 and osteocalcin were downegulated by 6, 11 and 5 folds respectively. Conclusions. Our study showed that MMV can induce expression of angiogenic and invasion genes and reduce expression of osteoblastic genes in MSC. This suggests presence of pro-tumorigenic activators and osteogenic inhibitors in MMV. Currently the biochemical composition of MMV is being assessed. We also noticed that MSC isolated from MM patients have skewed expression of several pro-tumorigenic and osteogenic genes in comparison to healthy controls. 1006 DIFFERENTIAL EXPRESSION OF CD13 IN BONE MARROW COMPARTMENTS OF CD34 + CELLS BETWEEN DIFFERENT GROUPS OF PATIENTS WITH MYELODYSPLASTIC SYNDROMES S. Matarraz, 1 A. Lopez, 1 C. Salvador, 2 N. Fernandez-Mosteirin, 2 M. Giralt, 2 A. Orfao1 1 Centro de Investigación del Cáncer, SALAMANCA, Spain; 2 Hematology ServiceMiguel Servet Hospital, ZARAGOZA, Spain Background. Aminopeptidase N (APN)/CD13 is a transmembrane protease present in a wide variety of human tissues and cell types (endothelial, epithelial, fibroblasts, leukocyte). This molecule is involved in extracellular proteolysis, regulation of chemokine and cytokine activity, and several other different cellular functions such us growth, secretion of angiogenic molecules, motility and apoptosis. Expression of CD13 has been shown to be deregulated in inflammatory as well as neoplastic diseases. CD13 is overexpressed in acute and chronic myeloid leukemias while information about its expression in myelodysplastic syndromes (MDS) patients is currently limited. Objective. In the present study we analyzed the expression of CD13 in normal myeloid CD34 + BM precursors as well as in CD34 + cells from BM of patients with MDS in order to evaluate the frequency of altered CD13 expression and its relationship with the World Health Organization (WHO) and International Prognostic Scoring System (IPSS) categories of MDS. Patient and methods. A total of 73 BM samples corresponding to 23 healthy individuals (control group), and 50 patients with newly diagnosed MDS were analyzed. Patients were classified according to the WHO and IPSS criteria into: refractory anemia (RA) (n=11), refractory cytopenia with multilineage dysplasia (RCMD) (n=9), RA with excess of blasts (RAEB)-1 (n=13), RAEB-2 (n=10), unclassifiable MDS (UNC) (n=2) and myelodysplastic/myeloproliferative disorder (MDS/MPD) (n=5). Low risk (LR) (n=12), intermediate risk (INT)-1 (n=14), INT-2 (n=9), and high risk (HIGH) (n=4); in 11 cases karyotypic information was not available. Among CD34 + BM cells three major cells subsets were identified: the more immature CD34 + precursors (PRin), CD34 + /cyMPO + cells already committed to neutrophil lineage (PRneu) and B-cell precursors. Expression of CD13 was analyzed by flow cytometry in the former two compartments of CD34 + precursors in terms of both percentage of CD13 + cells and the amount of expression/cell of this protein. Results. As compared to NBM, MDS patients showed overall increased percentages of CD13 + /CD34 + cells associated with higher amounts of CD13 expression 12 th Congress of the European Hematology Association in both the PRim and PRneu CD34 + cell subsets. Such increased CD13 expression was specifically observed for those groups of cases with a poor outcome such as AREB-2 and HIGH risk MDS patients (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.
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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
Page 329 and 330: 0862 COMPARISON OF DASATINIB TO HIG
Page 331 and 332: 0867 COMPREHENSIVE GERIATRIC ASSESS
Page 333 and 334: 0872 MN1 INDUCES LEUKEMIA IN MICE A
Page 335 and 336: 0877 PAX5/TEL TRANSDUCED PRE-BI CEL
Page 337 and 338: 0882 CISPLATIN INDUCES THROMBIN GEN
Page 339 and 340: have an early manifestation of typi
Page 341 and 342: 0892 INTEGRATION OF GENOME WIDE SNP
Page 343 and 344: 0897 THE PHENOTYPE OF JAK2V617F MUT
Page 345 and 346: 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
Page 351 and 352: BRIC 126 and 4N1K) in cells lacking
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Page 355 and 356: 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: 3 of disease relapse.TRM at day+100
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 and 408: patient is still undergoing intensi
Page 409 and 410: nificant MVD differences were detec
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
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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
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
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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
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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
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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
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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
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
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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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