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12 th Congress of the European Hematology Association anemia), therapeutic treatments (e.g. transplantations) and supportive care (e.g. transfusion support) will be requested in the future. Since most of the MDS patients are not eligible for transplantation it can be assumed that the economic burden of MDS is determined predominantly by anemia and transfusions. Aims. To describe the economic burden of transfusion and anemia in MDS on the basis of published literature. To make a first estimate of the economic impact for Germany. Methods. Literature search via PUBMED was systematically conducted (covering 1/96 to 12/06) using the search terms: Myelodysplastic Syndrome AND Transfusion AND Cost and cost analysis OR cost of illness OR health care costs OR epidemiology; anemia AND cancer AND cost OR transfusion. Further desk-top researches were conducted to evaluate the economic burden of transfusion-dependency of MDS patients from the German transfusion medicine’s perspective. Results. Three MDS cost-analyses focus on transfusion costs and present direct costs from the payers’ perspective. Regarding anemia in cancer patients 4 cost-of-illness analyses, 4 cost-effectiveness-analyses, 3 cost-minimisation analyses and 4 other cost analyses were identified. Most studies analyse the US-American situation from the payers’ perspective. Prevalence of MDS in Germany is estimated to range between 7,300 and 10,500 patients. Assuming a need of 24 erythrocytes per transfusion dependent MDS patient per year in average, MDS transfusions add up to 2 to 3 per cent of whole erythrocyte production in Germany in 2004. Depending on the current unit price of erythrocytes and the numbers of transfusion dependent MDS patients, the total costs of transfusion vary between 8 and 23.5 million Euro per year. The number of transfusion dependent MDS patients will grow by approximately 1,760 up to approx. 7,200 patients in Germany in 2010 resulting in transfusion costs between 15 and 30 million Euro. Summary and Conclusions. There is a lack of information on the economic burden of MDS. To evaluate the economic consequences of innovative therapeutics in MDS it is important to provide information of resource consumption and the respective costs on the basis of real life data. It is important to present the results by disease severity and treatment options. The treatment of transfusion dependent MDS is of special public health interest. Blood is an increasingly scarce and expensive resource and unnecessary transfusions may cause a shortage of blood products for patients in real need. Therefore the value of blood conserving strategies should be evaluated from a broader perspective - the societal perspective. 0842 PHARMACOGENOMIC APPROACH OF SICKLE CELL DISEASE TREATMENT: GLOBAL ANALYSIS OF HYDROXYUREA EFFECT ON HUMAN ENDOTHELIAL CELLS TRANSCRIPTOME S. Laurance, 1 A. Benecke, 2 E. Verger, 1 R. Krishnamoorthy, 1 J. Elion, 1 C. Lapoumeroulie1 1 UMR INSERM U763/Université Paris7, PARIS; 2 Institut des Hautes Etudes Scientifiques, BURES SUR YVETTES, France Background. The clinical hallmarks of sickle cell disease (SCD) are recurring painful vaso-occlusive episodes, chronic anaemia and multiple organ damages. Although the polymerisation of Haemoglobin S (HbS) is the base of the pathophysiology, the vascular endothelium seems to play an essential role in vascular occlusion. Hydroxyurea (HU) is the only drug with a measurable clinical benefit for SCD patients by reducing the frequency of vaso-occlusive crisis. Initially, HU was administrated to induce HbF expression but there is no link between the observed clinical benefit and the expected increase of HbF expression. Due to the crucial role of ECs in SCD, our laboratory investigates the effect of HU therapy on ECs. Indeed, we have shown that HU affects the expression of specific endothelial genes. These genes seem to be implicated in the pathobiology since they encode for adhesion molecules (VCAM-1), vaso-modulators (endothelin-1) and cytokines (Il-6, Il-8). Aims. We decided to pursue analysis of HU effect on endothelial cells in the way to identify HU targets genes and downstream pathways by establishment of differential transcriptome profiling of human ECs (cells exposed to HU vs unexposed). Methods. Our analysis was performed by a systematic screening of HU target genes based on the use of a micro-array system which allows to evalute the expression level of the whole human transcriptome since the array contains probes for 29,198 identified genes. We have analysed the effect of HU 24h treatment period on the transcriptome profile of a human endothelial cell line derived from bone marrow microcirculation (TrHBMEC). Results. The subtraction profile (HU vs non-treated) identifies 2448 potential novel target genes. RQ-PCR experiments were carried out to validate the method applied and these differentially expressed HU target genes. Among them, thrombospondin- 1 (TSP-1), von Willebrand factor (vWF), PECAM-1, AXL mRNA levels 314 | haematologica/the hematology journal | 2007; 92(s1) are decreased and interleukin-1 α and β mRNA are increased. All these factors seem to be relevant for the pathobiology and endothelium functions. In fact, TSP-1 and vWF are implicated in adherence and coagulation events and high levels of these two proteins are detected in SCD patients. PECAM-1 modulates vascular permeability and lymphocytes extravasation, AXL is a new vascular system regulator and is implicated in adhesion phenomenon. IL-1 α and β are pro-inflammatory cytokines; their up-regulation by HU is paradoxical with the improved clinical features. Experiments at the protein level are thus carried out to validate the mRNA data. Conclusion. Presently, we find, by an exhaustive transcriptome analysis, new relevant endothelial target genes of HU, however some of our results seem to be inconsistent with clinical benefits suggesting that SCD and its treatment are complex and require more experiments. The same type of microarrays experiments has also been carried out combining pro-inflammatory cytokines and hydroxyurea treatment in a way to simulate SCD inflammatory context. A global signaling pathway analysis of the data is performed to identify the biological processes and the molecular pathways affected by HU. A better understanding of HU molecular effects and downstream pathways should lead to the emergence of improved and more targeted therapies. 0843 ANGIOGENESIS AND PERYCYTE MARKERS IN SEVERE HEMOPHILIACS WITH DIFFERENT CLINICAL PHENOTYPES A. Calleri, 1 L. Saronni, 2 E. Biguzzi, 3 F. Franchi, 3 P. Mancuso, 2 C. Rabascio, 2 V. Raia, 2 M.E. Mancuso, 3 E. Santagostino, 3 P. Antoniotti, 2 J. Quarna, 2 P.M. Mannucci, 3 F. Bertolini2 1 European Institut of Oncology, MILAN; 2 European Institute of Oncology, MILAN; 3 Ospedale Maggiore di Milano, MILAN, Italy Background. Haemophilia is an inherited hemorrhagic disorder, characterized by spontaneous bleeding episodes. However, some severe haemophilic patients exhibit a mild bleeding tendency. It is possible to hypothesize that the vascular and perycyte component of haemostasis can influence the capacity of repairing vascular damage in these individuals. Aims. to investigate different surrogate markers of angiogenesis and vasculogenesis in haemophilic patients. Methods. Two groups of patients with severe haemophilia were enrolled: 11 mild bleeders (MB: ≥2 spontaneous bleeding episodes/year; concentrate use
0844 INCREASED LEUKOCYTE-PLATELET INTERACTIONS ASSOCIATED WITH HIGH RISK HEART SURGERY N.M. Matijevic, 1 A. Bracey, 2 B. Radovancevic, 2 R. Radovancevic, 2 I. Gregoric, 2 O. Frazier 2 1 University of Texas Health Science Cente, HOUSTON, TX; 2 Texas Heart Institute, HOUSTON, USA The role of circulating leukocytes and their interaction with platelets play an important role the hemostasis and inflammation. Leukocyteplatelet complex formation depends on the interaction between platelet P-selectin and leukocyte ligand P-selectin glycoprotein ligand-1 (PSGL- 1). Implantation of a left ventricular assist device (LVAD) is used to provide hemodynamic support in patients with severe heart failure. Bleeding, thromboembolism, and infections are common complications associated with LVAD. Cell activation and leukocyte-platelet interactions during LVAD implantation is reported in a limited number of studies. We measured circulating levels of monocyte-platelet complexes (MPC), granulocyte-platelet complexes (GPC), and lymphocyte-platelet complexes (LPC) in 11 patients who received LVAD support. Blood samples were collected before LVAD implantation, and at days 3, 7, 14, 21, 30, 60, 90, and 180. Flow cytometry was used to measure circulating heterotypic cell aggregates. The following antibodies were used: CD14, CD162 (PSGL-1), CD41(GPIIb), and CD62P (P-selectin). Monocytes were identified by specific staining with CD14 antibody, and lymphocytes and granulocytes were identified by their forward and side light scatter properties. The percentage of the leukocyte-platelet complexes was defined by their CD41 positivity. Baseline levels of PSGL-1 on monocytes were significantly higher than that on granulocytes and lymphocytes (160.6±21.5, 91.6±12.3, and 77.2±8.4), respectively. After transient increase on postoperative day 3, PSGL-1 surface expression showed persistent decreasing trends thereafter. The average percentages of the three types of leukocyte-platelet complexes were within normal range before implantation (9.1±2.5, 8.3±2.6, and 8.6±2.2, respectively). MPC and GPC increased significantly on day 7 (16.5±7.6 and 14.4±7.2), peaked on day 21 (26.9±11.7 and 25.4±8.8), and remained significantly elevated up to 60 days of the post implantation period. The average percentage of the LPC increased by day 14 and remained elevated thereafter. A significant inverse correlation was found between MPC and monocyte PSGL-1 (R=- 0.84), LPC and lymphocyte PSGL-1 (R=-0.78) and GPC and granulocyte PSGL-1 (R=-0.69), indicating increased levels of leukocyte and platelet activation. A significant positive correlation between MPC and CD14 (R= 0.6), further confirmed ongoing monocyte activation. The preliminary results of this pilot study documented an increased cellular activation and heterotypic cell interactions in patients undergoing high risk heart surgery. Circulating leukocyte-platelet complexes along with other markers of cell activation require correlation with longer follow-up of larger groups of patients and subsequent clinical events in order to understand its clinical significance. 0845 TRANSFUSION RATES AND PLATELET ACTIVATION IN PATIENTS UNDERGOING HIGH RISK CARDIAC SURGERY A. Bracey, 1 R. Radovancevic, 1 N. Matijevic, 2 B. Radovancevic, 1 S. Carranza, 1 I. Gregoric, 1 O. Frazier1 1 2 Texas Heart Institute, HOUSTON; Univesity of Texas Health Science Center, HOUSTON, USA Introduction. Left ventricular assist device (LVAD) implantation is associated with a high incidence of hemorrhagic complications, high-volume transfusion and reexploration rates for bleeding. Increased platelet activation in these patients is reported in a limited number of studies. We sought to determine the effect of preoperative platelet activation on bleeding and transfusion rates in this surgical procedure. Methods. We used flow cytometry methods to measure expression of the platelet activation markers in 11 patients (7 men, 4 women) with end stage heart failure who underwent LVAD implantation. P selectin (CD62P) and thrombospondin (TSP) levels were analyzed and compared to transfusion rates and bleeding. Data collected include: age, body weight, sex, intraaortic balloon pump insertion, previous cardiac surgery, creatinine, BUN, total bilirubin, and hemoglobin levels, PT, INR, PTT, platelet count, WBC count, and antifibrinolytic use. Results. Preoperatively, the average percentage of positive platelets was 26±13% for CD62P and 9.4±5.4% for TSP. Six patients with percent of positive platelets equal or greater than the median value for CD62P (23.7%) and TSP (9.5%) required more platelet transfusions (9.2±3.1 vs. 3.8± 2.9 units, p=0.015) and bled more 12 th Congress of the European Hematology Association (74±23 vs. 43±26 mL/kg, p=0.037). They also required more red blood cell units (11.3±4.4 vs. 6.8±3.9, p=0.052) and fresh frozen plasma units (14.7±5.6 vs. 6.2±4.1, p=0.035) than patients who had less activated platelets. Conclusions. These results on a limited number of patients suggest correlation of platelet activation with increased bleeding and transfusion requirements during LVAD implantation. Further study is warranted to confirm this finding. 0846 IMMUNE CELLS MIMIC THE MORPHOLOGY OF ENDOTHELIAL PROGENITOR COLONIES IN VITRO E. Rohde, 1 C. Bartmann, 2 K. Schallmoser, 1 A. Reinisch, 3 G. Lanzer, 1 W. Linkesch, 3 C. Guelly, 4 D. Strunk3 1 Div. of Transfusion Medicine, GRAZ; 2 Div. of Hematology; Transfusion Medicine, GRAZ; 3 Div. of Hemetology, GRAZ; 4 Center for Medical Research, GRAZ, Austria Background. Endothelial progenitor cells (EPC) are considered powerful biologic markers for vascular function and cardiovascular risk predicting events and death from cardiovascular causes. Colony-forming units of endothelial progenitor cells (CFU-EC) are used to quantify EPC circulating in human peripheral blood. The mechanisms underlying colony formation and the nature of the contributing cells are not clear. Methods. We performed subtractive CFU-EC analyses to determine the impact of various blood cell types and kinetics of protein and gene expression during colony formation. Results. We found that CFU-EC mainly comprise T cells and monocytes admixed with B cells and NK cells. The combination of purified T cells and monocytes formed CFU-EC structures. The lack of colonies after depletion or functional ablation of T cells or monocytes was contrasted with effective CFU-EC formation in the absence of CD34 + cells. Microarray analyses revealed activation of immune function-related biological processes without changes in angiogenesis-related processes during colony formation. In concordance with a regenerative function, soluble factors derived from CFU-EC cultures supported vascular network formation in vitro. Conclusions. Recognizing CFU-EC formation as the result of a functional cross between T cells and monocytes shifts expectations of vascular regenerative medicine. Our data support the move from a view of circulating EPC towards models that include a role for immune cells in vascular regeneration. 0847 EVALUATION OF RELEASED FACTORS, WITH A POTENTIAL POST-TRANSFUSION IMMUNOMODULATORY ROLE, DURING THE STORAGE OF PLATELET CONCENTRATES S. Misso, 1 L. Paesano, 2 M. D'Onofrio, 2 B. Feola, 1 C. Marotta, 1 G. Fratellanza3 , E. D'Agostino3 , A. Minerva1 1 Hospital S. Sebastiano and S. Anna, CASERTA; 2 Hospital S. Giovanni Bosco, NAPLES; 3 University Federico II, NAPLES, Italy Background. Platelets have a specialized role in haemostatic responses, in spite of this, new functions have been recently identified. In fact, the thrombocytes also participate in the process of inflammation by releasing different substances capable of modulating the whole inflammatory response by interactions with both endothelial and white blood cells. Recent studies have demonstrated that the platelets take part in immunity and inflammation mainly by means of the CD40/CD40L pathway. Aims. Our objective has been to evaluate the accumulation of cytokines, during the storage, in platelet concentrates obtained from platelet-rich plasma. Methods. Fifty platelet concentrates have been analyzed in Caserta’s Hospital; a plasma sample has been taken from every unit just after production of the hemocomponent (T.0) and after 1 (T.1), 3 (T.3), and 5 (T.5) days of storage (at 22±2°C in continuous agitation). IL-6, IL-8, PDGF-AA, sCD40L and leptin levels have been assayed by specific ELISA commercial kits (R&D Systems). Results. IL-6 (T.0= 6.3±1.9 pg/mL, T.1=7.1±2.6, T.3=9.3±3.1, T.5=10.2±3.9, p>0.05) and IL-8 (T.0=8.9±3.3 pg/mL, T.1=10.1±3.6, T.3=12.3±4.1, T.5=16.8±6.4, p>0.05) levels have been stable during all the storage with no statistical significant variation. On the other hand, PDGF-AA (T.0=210±20 pg/mL, T.1=298±36, T.3=463±29, T.5=690±47, 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
Page 271 and 272: 0705 THE SHIFT OF TREATMENT FOR NAS
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Page 275 and 276: patients presented a stage IV disea
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Page 279 and 280: known at NHL diagnosis, were includ
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Page 289 and 290: 0753 A SUSTAINED REMISSION OF IDIOP
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Page 295 and 296: Results. A total of 396 patients we
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Page 309 and 310: p=0.014 and p=0.003, respectively).
Page 311 and 312: 0809 CURRENT APPROACH TO CHELATION
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Page 315 and 316: the 97.5th percentile (5.2 U/mL) ge
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Page 319 and 320: Transfusion medicine and vascular b
Page 321: tions (most bacterial, 2 malaria, 6
Page 325 and 326: 0851 CORD BLOOD DERIVED MESENCHYMAL
Page 327 and 328: 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
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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
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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
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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
Page 453 and 454:
1217 INCIDENCE OF EARLY STAGE IDIOP
Page 455 and 456:
1691GA and 1 homozygous 1691AA. The
Page 457 and 458:
1230 ASSOCIATION OF HEPARANASE GENE
Page 459 and 460:
posed, was: DF = (CD43%+FMC7%+CD79b
Page 461 and 462:
treatment of acute promyelocityc le
Page 463 and 464:
loaded group and 35 (70%) were non-
Page 465 and 466:
mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
Page 469 and 470:
ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
Page 475 and 476:
disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
Page 479 and 480:
phamide 750 mg/m 2 on day 1, vincri
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
Page 497 and 498:
Results. Though there was no recogn
Page 499 and 500:
2% and 19% of patients with or with
Page 501 and 502:
were older than 65 y) which can be
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
Page 505 and 506:
median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
Page 509 and 510:
to the presence of IVS1-6 mutation
Page 511 and 512:
fy predictive factors for these abn
Page 513 and 514:
acute leukemia. However, we cannot
Page 515 and 516:
agents. They involve primarily the
Page 517 and 518:
voriconazole for 2 months followed
Page 519 and 520:
typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
Page 523 and 524:
with development of BC/AP. 2. EVI-1
Page 525 and 526:
1447 THE IMPACT OF DISPARITY IN SHO
Page 527 and 528:
three had visual field defects, two
Page 529 and 530:
acquired mutation most prone to cau
Page 531 and 532:
1466 ROS GENERATION AND APOPTOSIS I
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
Page 545 and 546:
Hodgkin’s disease is well known,
Page 547 and 548:
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
Page 557 and 558:
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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