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12 th Congress of the European Hematology Association dence of bulky disease was higher in pts with IPS 3-5 than in pts with IPS 0,1. (23.3% vs 6.6% p50 was found in pts with IPS 3-5 comparing to the pts with IPS 0.1 (33.3% vs 10% p50 found in pts with high IPS pointed out shorter survival of those pts (40.86 m vs 64.4 m p3, bulky disease and ESR>50 are in risk of relapse and treatment failure, and are eligible for the initial aggressive therapeutic approach. 1073 FLAG-IDA IN THE TREATMENT OF REFRACTORY/RELAPSED ACUTE LEUKEMIA: A SINGLE INSTITUTIONAL STUDY P. Carluccio, 1 D. Pastore, 1 A. Pannunzio, 1 A. Russo Rossi, 1 P. Lerario, 1 G. Spinosa, 1 M. Giannoccaro, 1 A.M. Mazzone, 1 M. Santodirocco, 2 V. Fesce, 2 C. Lubelli, 1 A. Liso, 2 V. Liso, 1 G. Specchia1 1 Hematology Section, BARI, Italy; 2 Hematology, FOGGIA, Italy Background. Relapsed or refractory adult acute myeloid leukaemia (AML) have a poor prognosis. The strategy for treating this patients is through reinduction chemotherapy followed by allogeneic stem cell transplantation, provided that the toxicity of the salvage regimen is acceptable. High or intermediate dose cytarabine has been reported to be effective in the salvage treatment of AML; addition of the purine analogue fludarabine to cytarabine increases the rate of accumulation of cytarabine in leukemic blasts and the response to chemotherapy may be improved by addition of idarubicin, an anthracycline that is less susceptible to multidrug resistance Aims. Based on these consideration, we evaluated the efficacy and the toxicity of FLAG-IDA in a series of 78 refractory/relapsed AML. Patients and Methods. Fifty-two patients (66%) were in first relapse and 26 (34%) were refractory to conventional chemotherapy. The patient group included 44 men and 34 female with a median age of 43 years (range 15-63). All patients were treated with fludarabine (30 mg/m 2 iv for 5 days), cytarabine (2 gr/m 2 iv for 5 days), idarubicin (10 mg/m 2 iv for 3 days) and G-CSF (5 mcg/Kg/day subcutaneous 24 h after completing chemotherapy and until neutrophil regeneration). Results. The overall CR rate was 55% (43 of 78): 31 of 52 (59%) in relapsed and 12 of 26 (46%) in refractory patients; there were 5 of 78 (6%) deaths during therapy: 2 due to cerebral haemorrhage and 3 due to infection. In patients achieving remission, the median time to reach absolute neutrophil count (ANC) more than 0.5×10 9 /L and 1×10 9 /L was 21 (range 16-26) and 24 days (range 20-28) from the start of chemotherapy, respectively. Platelets level of more than 20 ×10 9 /L and 100 ×10 9 /L were achieved in a median time of 24 (range 19-26) and 32 days (range 28-39) days, respectively. Fever more than 38.5°C was observed in 63 of 78 patients (80%): 45 (71%) had fever of unknown origin and 18 (29%) documented infections. Nonhematological side effects, consisting mainly of mucositis (60/78 or 76%) and transient liver toxicity increase (30/78 or 38%). All 43 patients who achieved CR received a second course with FLAG-IDA, and 18 received allogeneic stem cell transplantation, 8 patients received autologous stem cell transplantation, 9 were junged unable to receive any further therapy, and 8 refused other therapy. The median overall survival (OS) for all 78 patients was 6 months (range 3- 62); for the 43 responders patients, the disease free survival (DFS) and OS were 9 (range 4-62) and 11 (range 7-62) months, respectively; the 18 patients who received allogeneic transplantation had a DFS of 13 (range 7-62) months. Summary. In our experience, FLAG-IDA is a well-tolerated regimen in refractory/relapsed AML with a CR rate of 55%; the toxicity of this treatment is acceptable, enabling the patients who achieved CR to receive further treatment, including transplantation procedures. 1074 POLYMORPHISMS OF DNA REPAIR AND DETOXIFICATION GENES IN B-CELL CHRONIC LYMPHOCYTIC LEUKAEMIA C. Ganster, 1 J. Neesen, 1 U. Jaeger, 2 H. Esterbauer, 3 C. Mannhalter, 3 C. Fonatsch1 1 Department of Medical Genetics, MUW, VIENNA, Austria; 2 Department of Internal Medicine I, MUW, VIENNA, Austria; 3 KIMCL, MUW, VIENNA, Austria B-cell chronic lymphocytic leukemia (CLL) is the most common type of leukemia in adults in the Western World. As its clinical course is highly variable, prognostic factors for disease progression such as particular cytogenetic abnormalities, the mutational status of the immunoglobulin heavy chain (IgH) genes, LPL, or CD38 expression, have been identified. However, a convincing prediction of disease progression can not 396 | haematologica/the hematology journal | 2007; 92(s1) be made in early stages of the disease. Further prognostic factors would be helpful for meaningful prediction of disease progression. There is evidence that multiple low-penetrance genetic factors, including genetic polymorphisms, predispose to CLL or modify its clinical course. The aim of this study was to identify such allelic variants of genes, primarily concentrating on DNA repair and detoxification genes. We studied the distribution of 50 polymorphisms in 500 CLL-patients and 500 control persons using PCR amplification followed by restriction enzyme digestion. Whereas for most polymorphisms an association with CLL could be excluded, the risk of the development of CLL increased with the number of high-risk alleles in the DNA base excision repair gene XRCC1 and in a combined analysis on alleles in XRCC1 and the detoxification gene CYP1B1. Further investigations are now under way to proof the relevance of these polymorphisms in the clinical course of CLL and its putative significance for CLL in combination with other prognostic factors. The results of this study will lead to new insights into the etiology of CLL and may help to predict disease progression. 1075 THRESHOLDS OF IRON TOXICITY IN PATIENTS OF MYELODYSPLASTIC SYNDROMES H. Brummendorf, 1 P. Nielsen, 1 N. Kroeger, 1 R. Grosse, 1 J. Matt, 2 R. Engelhardt, 1 O. Leismann, 2 C. Bokemeyer, 1 R. Fischer, 1 A. Zander, 1 T. Brummendorf1 1 University Hospital Eppendorf, HAMBURG, Germany; 2 Novartis Pharma GmbH, NÜRNBERG, Germany Background. Patients with myelodysplasia (MDS), osteomyelofibrosis (OMF), or severe aplastic anemia (SAA) suffer from ineffective erythropoiesis due to pancytopenia, which is often treated with red blood cell transfusion. Especially in low-risk patients with mean survival times of > 5 years (MDS-RA, -RARS, -5q-), potentially toxic levels of liver iron concentration (LIC) can be reached. Aims. Although, the 2005 consensus of Nagasaki gave recommendations for chelation treatment based on a wide range of ferritin levels, there is still no evidence based agreement about the initiation of chelation treatment in these patients. Moreover, ferritin levels can vary independently from the true iron stores as assessed by LIC. Therefore, we aimed to establish a relationship between LIC and ferritin in the patients of the myelodysplasia syndrome. Methods. In the present study, a total of 67 transfused patients with MDS (n=20, age: 17-75 y), OMF (n=4, age: 48-68 y), SAA (n=43, age: 5-64 y) were measured by SQUID biomagnetic liver susceptometry (BLS) and their liver and spleen volumes were scanned by sonography at the Hamburg biosusceptometer. Less than 50% were treated with DFO. LIC (µg/g-liver wet weight, conversion factor of about 6 for µg/g-dry weight) and volume data were retrospectively analyzed in comparison to ferritin values. Results. LIC values ranged from 149 to 8404 with a median value of 2705 µg/g-liver, while serum ferritin (SF) concentrations were between 500 and 10396 µg/l with a median ratio of SF/LIC = 0.9 [(µg/L)/(µg/g-liver)] (range: 0.4 to 5.2). The Spearman rank correlation between SF and LIC was found to be highly significant (RS=0.80, p 2700 µg/g-liver (Angelucci et al. Blood 2002; 100:17-21) within 60 months and significant cardiac iron levels have been observed for LIC > 3300 µg/g-liver (Jensen et al. Blood 2003; 101:4632-9). These thresholds were exceeded by 51% and 39% of our patients for hepatic fibrosis progression and for cardiac iron toxicity, respectively. The total body iron burden is even higher as more than 50% of the patients had hepatomegaly (median hepatomegaly factor: 1.2 of normal). Summary/Conclusions. A liver iron concentration of about 3000 µg/g-liver or 18 mg/g-dry weight has to be seen as the latest intervention threshold for chelation treatment as MDS patients are affected by more than one risk factor. A more secure intervention threshold would be a LIC of 1000 µg/g-liver or 4 - 6 mg/g-dry weight, corresponding with a ferritin level of 900 µg/L for transfused MDS patients. Such a LIC value is not exceeded by most of the heterozygous hereditary hemochromatosis subjects and is normally well tolerated without treatment during their life-time.
1076 SERUM LEVELS OF SOLUBLE HLA CLASS-I MOLECULES, ICTP, AND RANKL AS PROGNOS- TIC PARAMETERS IN MULTIPLE MYELOMA PATIENTS P. Schutt, 1 V. Rebmann, 1 D. Brandhorst, 1 J. Wiefelspütz, 1 P. Ebeling, 1 B. Opalka, 1 S. Seeber, 1 M.R. Nowrousian, 1 H. Grosse-Wilde, 2 T. Moritz 1 1 University of Essen, ESSEN, Germany; 2 Institute of Immunology, ESSEN, Ger- many Given the highly variable clinical course of multiple myeloma, the analysis of prognostic parameters bears considerable clinical interest. We here have analyzed the clinical significance of serum levels of soluble HLA class I molecules (sHLA-I), carboxy-terminal telopeptide of type- I collagen (ICTP), and receptor activator of nuclear factor kappa B ligand (RANKL). sHLA-I (median, range in µg/L) were significantly (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
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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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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
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 and 380: 3 of disease relapse.TRM at day+100
Page 381 and 382: survival of five years. This dismal
Page 383 and 384: 1011 FLOW CYTOMETRIC DNA INDEX AND
Page 385 and 386: 1018 THE EFFECT OF THE SUGARBAKER P
Page 387 and 388: 1024 KIR/HLA CLASS I MISMATCHING AN
Page 389 and 390: ment details and thrombotic histori
Page 391 and 392: 1036 INCIDENCE AND SPECTRUM OF INFE
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: 1069 CLINICAL RELEVANCE OF REGULATO
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 and 452: efficacy and decreased atherosclero
Page 453 and 454: 1217 INCIDENCE OF EARLY STAGE IDIOP
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1691GA and 1 homozygous 1691AA. The
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1230 ASSOCIATION OF HEPARANASE GENE
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posed, was: DF = (CD43%+FMC7%+CD79b
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treatment of acute promyelocityc le
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loaded group and 35 (70%) were non-
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mild. Fas and soluble Fas ligand le
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1265 POSACONAZOLE THERAPY IN REFRAC
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ly express the cytoplasmic (inactiv
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findings confirmed the significant
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a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
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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
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esulting alterations of the endothe
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(range 1-7) and 28,6% of patients h
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three decades. In vivo, Ara-C is tr
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statistical analysis. Results. Seve
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Results. Though there was no recogn
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2% and 19% of patients with or with
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were older than 65 y) which can be
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1376 RESVERATROL INDUCED P53 MEDIAT
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median time of 21 days to reach >0.
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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,
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Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
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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
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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.,
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Lin, L.-I., 0030, 0484 Lin, T., 012
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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
Page 595 and 596:
Zouabi, H., 0503, 0999 Zoumbos, N.C
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12th Congress of the European Hematology ... - Haematologica

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