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12 th Congress of the European Hematology Association gene were detected with PCR followed by digestion with EcoRV of the 114 bp PCR product (PCR band(s) 68 and 46bp for wild type). Non fully digested products were considered as mutated. Results. The median age of onset was 47±12 (range from18-75) years, (116 males and 86 females).FLT3-ITD were detected in 36/202 patients (18%) and D835 mutations in 12/202 (6%). In the study group of 202 patients according to FAB classification, rate of FLT3 mutations were found higher in M3 with 40/176 (22.7%). The distribution of FLT3 mutations was as follows: FLT3-ITD was detected in M2 2/8 (25%) patients, in M3 32/176 (18.2%), in M4 2/8 (25%). D835 mutation was found in 8 patients with M3 and 4 patients with M2 and M5 type of AML. The majority cases were acute promyelocyte leukaemia and characterized by the T-15-17. Evidence to date suggest that PML/RARA is insufficient for leukomogenesis. Potential candidate include mutations of FLT3, which could confer a proliferative advantage thereby complementing the differentiation block induced by PML-RARA. There was no correlation between patients with ITD status and gender and age. A positive correlation with high presenting WBC > 20000/micl (58%) and high percentage of circulating blast cells was demonstrated in ITD positive patients (p
1217 INCIDENCE OF EARLY STAGE IDIOPATHIC MYELOFIBROSIS: SINGLE INSTITUTION EXPERIENCE G. Mele, P. Boccassini, M. Girasoli, C. Cristofalo, M.R. Coppi, C.M. Brocca, A. Melpignano, G. Quarta Antonio Perrino Hospital, BRINDISI, Italy Background. Early stage idiopathic myelofibrosis with associated thrombocytosis (i.e. prefibrotic myelofibrosis and early idiopathic myelofibrosis) are with difficulty distinguished from true essential thrombocytemia because of the high platelet count-sometimes greater than 1.000 × 109 /Las well as the lack of specific diagnostic markers (i.e. evident splenomegaly; high serum levels of LDH; circulating immature myeloid cells, erythroblasts and dacryocytes). In these select circumstances, only bone marrow features unequivocally help distinguish true essential thrombocytemia from early stage idiopathic myelofibrosis with associated thrombocytosis. In essential thrombocytemia megakaryocytes are mostly giant and contain an enlarged nucleus with deep lobulations, but lack the cytological abnormalities. In prefibrotic or early idiopathic myelofibrosis megakaryocytes present bizarre forms with marked nuclear-cytoplasmic anomalies. These evident dysplastic features exert a significant impact on prognosis and life expectancy; in fact, life expectancy is normal in true essential thrombocytemia but significantly shortened in prefibrotic myelofibrosis as well as in the various fibrotic stages of myelofibrosis. In addition, prefibrotic stages account for about 20-25% of all idiopathic myelofibrosis. Methods and Results. We have evaluated the incidence of early stages in our adult patients affected by idiopathic myelofibrosis. The data of 32 patients (19 males, 13 females; median age 71 years [range 35-84]) were retrospectively analysed; 7 patients (22%) were affected by early stage idiopathic myelofibrosis (4 prefibrotic myelofibrosis, 3 early idiopathic myelofibrosis). Analysis was focused on the discriminating impact of bone marrow and peripheral blood morphology. Our patients with early stage idiopathic myelofibrosis showed at diagnosis pronounced thrombocythemia (median value 879×109 /L [range 427’1.654]). The number of WBC was not significantly elevated (median value 13×109 /L [range 6-15]). Morphological examination of peripheral blood did not show evidence of immature myeloid cells or erythroblasts; the red blood cells were normocromic and normocytic in all patients however minimal anisocytosis was observed during the course of disease; in addition, peripheral blood smear showed frequently macro-platelets, agranular platelets and small aggregates. The bone marrow biopsies were hypercellular and dominated by atypical immature megakaryocytes, conspicuously large due to an increase of nuclear and cellular size, and always grouped in clusters of four/six elements; reticulin fibrosis was minimal (MF1) or absent (MF0). At diagnosis and during overall clinical follow-up all patients were asymptomatic: in fact they did not present fatigue, pruritus, fever, weight loss, bone pain, night sweats, spleen pain. Physical exam and abdominal echography detected occasionally very small splenomegaly. Cytogenetic analysis revealed a normal kariotype. LDH serum levels were normal. Conclusion. 1) In our Institution the incidence of early stage of idiopathic myelofibrosis is similar to that of international reports; 2) prefibrotic or early idiopathic myelofibrosis are characterized by a relatively indolent clinical course; 3) in view of the lack of specific diagnostic markers a detailed evaluation of bone marrow findings, particularly megakaryopoiesis, is recommended for a differential diagnosis between true essential thrombocytemia and prefibrotic or early idiopathic myelofibrosis with associated thrombocytosis; abnormal megakaryopoiesis offers the possibility of identifying early stages idiopathic myelofibrosis apart from the platelet count, laboratory parameters and clinical symptoms. 1218 HIGH DOSE SEQUENTIAL CHEMOTHERAPY AS SALVAGE TREATMENT FOR RELAPSED AND REFRACTORY HODGKINS LYMPHOMA L. Nassi, L. Rigacci, S. Guidi, L. Lombardini, C. Nozzoli, A. Gozzini, S. Mappa, B. Puccini, V. Carrai, R. Alterini, R. Saccardi, A. Bosi Careggi Hospital, FL, Italy Background. The optimal approach for patients with Hodgkin’s lymphoma (HD) who do not achieve a complete remission (CR) or relapse after induction therapy is still not definite. High-dose chemotherapy with autologous stem cell rescue proved to be more effective than conventional schemes considering the number of second CR and the duration of response. The German Hodgkin Study Group obtained good results with high-dose sequential chemotherapy (HDST) and autologous stem cell transplantation (ASCT) in this subset of patients. Aims. Evaluate the 12 th Congress of the European Hematology Association impact of HDST in relapsed and refractory HD patients. Methods. Since March 2002 to July 2006 16 patients were enrolled in this study in our institution. The schedule was constituted by a first phase (2 cycles of DHAP), a second phase (cyclophosphamide 4g/sqm, methotrexate 8 g/sqm, etoposide 2 g/sqm every 14 days) and an ASCT with BEAM conditioning. All phases but the ASCT one were delivered on outpatient basis. After the first phase a CT evaluation was performed to assess the chemosensibility: patients not achieving at least a partial response (PR) according to Cheson were considered off-study. Leukapheresis was performed after high-dose cyclophosphamide, and G-CSF 5 microg/Kg was administered from day +5 until collection. Results. Patients status at the enrolment were: 7 relapsed within an year after the obtainment of CR;7 refractory to the induction therapy (ABVD); 2 refractory to conventional salvage treatment for relapse occurred after 9 years. Characteristics of the patients at diagnosis were: median age 28 years (range 19-42); 8 patients were female; 7 had B symptoms; ECOG performance status were 0 in 10 patients, 1 in five, 2 in one. All patients received the two cycles of DHAP without delays. After this phase 7 patients were excluded, 5 for stable/progressive disease, 2 for not achieving a PR (the late relapsed patients, who are still alive with disease). Nine patients completed the therapy according to the schedule, and after the ASCT all of them were in CR with negative PET scans. A CR patient developed a myelodisplastic syndrome 13 months after the ASCT and died from acute graft versus host disease; a patient relapsed after 139 days, and died of progressive disease. The other seven patients are still alive and maintain the CR. Median time to treatment failure for the nine patients who completed the HDST was 31 months (range 139 days-52 months). Conclusions. HDST is an effective therapy for treatment of relapsed and refractory Hodgkin’s lymphoma. We observed a better outcome in the relapsed patients than in the primary refractory ones. After a median observation of more than 30 months we observed only a case of myelotoxicity, but a longer followup could better evaluate the real toxicity of this treatment. 1219 INHIBITORS IN HEMOPHILIA A AND B IN SOUTEAST OF TURKEY S. Pasa, A. Altintas, T. Cil, Y. Atayan, O. Ayyildiz Dicle University Medical Faculty, DIYARBAKIR, Turkey Background. The most important treatment related complication in hemophiliacs is inhibitor development. We evaluate the inhibitor developing rate of our patients, and discuss the possible reasons of low inhibitor development rates of them. Materials and Methods. We performed inhibitor screening of 99 hemophiliacs. Patients with < 1% of clotting factor activities were classified as severe, 1-5% moderate, and > 5-25% mild degree. Standart Bethesda procedure was performed for inhibitor screening, and used of 0.6 units as cut-off level. Results. Out of 99 patients; 84 were hemophilia A (84.8%), and 15 were hemophilia B (15.2%). Out of 84 hemophilia A patients; 53 (63.1%) were severe, 24 (28.5%) were moderate, and 7 (8.4%) were mild hemophilia A. Out of 15 hemophilia B patients; 8 (53.3%) were severe, 5 (33.4%) were moderate, and 2 (13.3) were mild hemophilia B. Only one hemophilia A patient was inhibitor positive (1.2% in severe hemophilia A), followed in our service with severe intraabdominal bleeding. None of hemophilia B patients have inhibitor. Conclusions. Expected inhibitor development incidence in hemophilia A and B approaches 33% and 3% respectively. Risk factors for inhibitory development may be patient and/or treatment-related. Our patients inhibitor prevalence was lower than previous studies. Factors that may responsible from this results; non of our patients were administered prophylactic factor concentrates, using fresh frozen plasma instead of factor concentrates. Inhibitor development become an important problem in our region with increasing availability of factor concentrates in prophylaxis and bleeding episodes. 1220 EFFECT OF PALIFERMIN ON THE INCIDENCE OF MUCOSITIS, HOSPITAL STAY, ACUTE GVHD AND TOTAL PARENTERAL NUTRITION IN PATIENTS UNDERGOING STEM CELL TRANSPLANTATION N. D’Cunha, B. Williams, M. Chriva-Internati, E. Cobos Texas Tech University, Health Sc Ctr, LUBBOCK, TEXAS, USA Kepivance is a keratinocyte growth factor (KGF) which stimulates the growth of cells in skin, mouth, stomach and colon. It has been suggested that Kepivance may reduce the incidence and severity of oral mucositis in patients receiving total body irradiation (TBI) conditioning regimen followed by autologous stem cell rescue. Very few studies have shown the effect of Kepivance on chemotherapy induced mucositis in patients haematologica/the hematology journal | 2007; 92(s1) | 445
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haematologica the hematology journa
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Information for readers, authors an
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EHA Executive Board E. Hellström-L
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Poster session I POSTER SESSION POS
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12 th Congress of the European Hema
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dasatinib. Methods. We studied Ikar
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Expression of the oncogene H-Ras an
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is the gene for the erythropoietin
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safety of a slow-release liposomal
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0029 OUTCOME OF THE TREATMENT OF AD
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drug-induced apoptotic response of
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41% in the PI3K- group (p=0.001). I
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Acute myeloid leukemia - Clinical I
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to 60 years (n=116, or 72%) receive
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0056 PROGNOSTIC SIGNIFICANCE OF FLT
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Anemia and Bone marrow failure 0061
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tified with the current protocol. S
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new cases of lead poisoning due to
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icance, from baseline to week 6 (p
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0086 THROMBELASTOGRAPHIC CHART RELI
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trials. The aim of this retrospecti
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tant function in this disease, nega
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ed to a favorable outcome. Bialleli
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stronger levels of p21 in the cell
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hematological centers in one countr
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ure 1). Conclusions. Results for re
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patients. After a median follow-up
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Cytogenetics and Molecular diagnost
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0135 ROUTINE DETECTION OF CYTOGENET
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(MMolR, defined as a BCR-ABL x 100
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0146 ARSENIC TRIOXIDE INDUCES ACCUM
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tinguish between genotypic B-cell l
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Genomics and proteomics 0158 PLASMA
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0164 EVALUATION OF MULTIPLEX LIGATI
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each patient’s replicate conditio
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0174 RELATION BETWEEN LOW PML-RARα
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0179 ESHAP VS GIN AS SALVAGE AND MO
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Immunology and gene therapy 0184 EA
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Cell viability was not affected by
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month is not relevant to chronic Gv
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Infection and supportive care I 020
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0206 POTENTIAL ROLE OF CMV IN THE O
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3H-thymidine uptake in cell culture
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0217 TUBERCULOSIS AMONG A COHORT OF
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0222 COMPARISON OF IWG 2006 AND IWG
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tem (IPSS) to h-MDS was also invest
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PCH97-19) were studied. Conventiona
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of erythroid colonies was reduced i
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0245 POTENT AND SELECTIVE INHIBITIO
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0250 INACTIVATION OF SUPPRESSOR OF
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Bortezomib 1.3 mg/m 2 days 1,4,8,11
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Response was defined according to E
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G-CSF can be used in neutropenic pa
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ence and functional activity of CD8
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itating tumor development, or engag
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phoma and SNT-13, -15 were establis
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usage (2/20 ie 10%) were observed.
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0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
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(range, 1-6) and 11 treatment cycle
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0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
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functional activity was confirmed b
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No major toxicity, neither hematolo
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enewal potential of X-RAR-positive
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(50-99) respectively. Serial analys
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cell-interaction, adhesion and acti
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0340 ALTERED FIBRIN CLOT STRUCTURE
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Conclusions. This study demonstrate
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0354 FACTOR V LEIDEN HOMOZYGOUS GEN
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Results. From July 2005 through Mar
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0364 CLINICAL EFFICACY OF OXALIPLAT
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one marrow and peripheral blood ste
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ecently suggested (Boissel et al.,
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0378 SAFETY AND EFFICACY OF THE TER
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Cytogenetics and molecular diagnost
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0385 CYTOPLASMIC MUTATED NUCLEOPHOS
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0390 ELTROMBOPAG RAISES PLATELET CO
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factor for the achievement of CR wa
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The cases of RAS showed two peaks o
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is 85%. Seven out of the 25 relapse
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0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
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successfully managed with GM-CSF di
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49% for PCR positive patients (95%
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+8 (1 PR+1 HI) and 14/24 pts with c
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(e.g. bcr-abl leading to CML). CSC
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0438 TERC MUTATIONS ANALYSIS IN PAT
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observed in all mice. Analysis of l
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ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
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One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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genesis of acute myeloid leukaemia
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polymorphism at nucleotide 4889 of
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expression along with a decreased C
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0487 MUTATIONAL STATUS OF NUCLEOPHO
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previously reported, a single cours
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0497 SINGLE AGENT CLORETAZINE (VNP4
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ly received melphalan-based chemoth
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were similar among the 3 groups. Ho
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Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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0523 DNA REPAIR INHIBITION IN RESTO
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held true when BMI-1 expression was
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Ph + cells in the bone marrow). We
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derivative chromosome (4p16, 7p14,
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0545 STABILIZED BONE MARROW IS NOT
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obtained in low (Sokal) risk patien
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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patients had died of their underlyi
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scripts and proteins most affected
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modulated after 24 h (37 up- and 59
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0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
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Results. A total of 396 patients we
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C30 questionnaire, and the correspo
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wave length of light of reflected r
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0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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BRIC 126 and 4N1K) in cells lacking
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sclerosis[NS] and 12 Mixed cellular
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0927 MK-0457, A NOVEL MULTIKINASE I
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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
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
Page 431 and 432: characterized in 198 β thalassaemi
Page 433 and 434: 1155 PLATELET AGGREGATION IN CHILDR
Page 435 and 436: to-pelvic or perineal trauma. No me
Page 437 and 438: in age. High prevalence of LBM amon
Page 439 and 440: ecause some of the patients were or
Page 441 and 442: of the drug is crucial to allow lon
Page 443 and 444: egarding cost analysis of ASCT in G
Page 445 and 446: ID Allo-BMT, 1 family one mismatche
Page 447 and 448: admitted to ICU were discharged des
Page 449 and 450: events -Postoperative states: 9,19%
Page 451: efficacy and decreased atherosclero
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
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1376 RESVERATROL INDUCED P53 MEDIAT
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median time of 21 days to reach >0.
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ly. Conclusions. 1. Combined intens
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to the presence of IVS1-6 mutation
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fy predictive factors for these abn
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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
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low up of ABL KD mutations’ level
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with development of BC/AP. 2. EVI-1
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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
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gene fusion is an independent progn
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1484 EPIDEMIOLOGY AND RESPONSE TO T
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1492 FREQUENCY OF MEDITERRANEAN GLU
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immune globulin was administered at
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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
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1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
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Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
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El-Sharkawy, N., 0016 Elwahidi, G.,
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Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
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Jaksic, B., 0127, 0446 Jaksic, O.,
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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,
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Musto, P., 0254, 0401, 0422, 0569,
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Papadavid, E., 1442 Papageorgiou, E
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Probatova, N., 0704 Prochazka, V.,
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Rykavicin, O., 0504 Ryningen, A., 0
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Sirard, C., 0127, 0128 Sirigou, A.,
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Thiebaut, A., 0454 Thieblemont, C.,
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Vincenzi, C., 1060 Viniou, N.-A., 0
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Zouabi, H., 0503, 0999 Zoumbos, N.C
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12th Congress of the European Hematology ... - Haematologica

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