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12 th Congress of the European Hematology Association unknown significance were identified in single cases. Mutations could be separated into 3 distinct patterns based on CE mutant quantification: low (6 cases < 30% mutant), intermediate (15 cases 30-60% mutant) and high (9 cases > 70% mutant) mutation load. There was no significant difference in the frequency of FLT3-ITD (47% Vs 34%) and NPM mutation (50% vs 62%) between WT1(M) and WT1(WT) cases. Patients with mutations in WT1 had an inferior initial response to therapy (Complete Remission [CR] WT1(M) 75% Vs WT1(WT) 90%, Odds Ratio [OR] 4.04, Confidence Intervals [CI] 1.30-12.5; p=0.02) and a higher rate of Resistant Disease [RD] (RD WT1(M) 16% Vs WT1(WT) 5%, OR 5.85, CI 1.29-26.4; p=0.02). Although Overall Survival (OS 34% vs 47%) and Disease Free Survival (DFS 33% vs 47%) were lower in the WT1(M) Vs WT1(WT) cases, this did not reach statistical significance. CE mutation analysis in 67 AML cell lines yielded mutation in the UF-1 (PML-RARA) and CTS (MLL-AF6) cell lines suggesting that WT1 mutations are likely to occur in other cytogenetic risk groups. Conclusions. WT1 mutations occur in 11% of NK AML at diagnosis. Mutations result in insertion or deletions in the DNA binding domain of the protein and have the potential to interfere with WT1 derived minimal residual disease detection. The locations of the common epitopes used for immunotherapy locate outside of the mutated region. WT1 mutations are associated with a lower CR rate and a higher rate of RD. Although OS and DFS are lower in the mutated group, this did not reach significance. Additional cases are being investigated to determine whether WT1 mutation status warrants inclusion as a poor risk marker in AML. 0054 ANALYSIS OF NPM1 MUTATIONS USING A SIMPLIFIED DNA-BASED PCR APPROACH DEMONSTRATES THAT ONE THIRD OF YOUNGER ADULT PATIENTS WITH NORMAL KARYOTYPE CARRY A MUTATION D. Rund, M. Safrai, M. Kedmi, S. Bar Cohen Hebrew University-Hadassah Hospital, JERUSALEM, Israel Background. There is a need for guidelines to improve risk stratification of patients with AML who have a normal karyotype. In 1999, it was discovered that rearrangements of the FLT3 gene confer a poor prognosis in AML. These were found in around 25% of AML, mostly in patients with a normal karyotype. In 2005, it was discovered that mutations in the NPM1 gene conferred a favorable prognosis. Analysis of these two mutations greatly improves prognostic ability for normal karyotype AML. The analysis of NPM1 mutations has generally been performed using histochemistry, sequencing of DNA, or RNA-based methods (RT- PCR) however many laboratories do not have the facilities to perform these analyses. Furthermore, as FLT3 analysis is performed on DNA, it is advantageous to have a DNA-based method to study these two aberrations in parallel. Aims. To establish and test a DNA-based method of NPM1 analysis. Methods. We have developed a DNA-based method for NPM1 analysis using PCR and melting temperature which gives rapid clearcut results which demonstrate the presence of a mutation. Although this method does not detect the specific type of mutation, this does not influence prognosis, and it is not crucial to determine it. We have used this method to analyze 154 patients with AML (primary and secondary) for both NPM1 and FLT3 mutations. 60 of these had a normal karyotype. FLT3 length mutations were analyzed by PCR and acrylamide gel electrphoresis. Results. Figure 1 shows a typical result of such an analysis. The tracing with a single peak represents normal DNA. The tracing with two peaks represents an AML patient sample which carries an NPM1 mutation. Figure 1. Melting curve analysis for NPM1 mutations. In total, we found that 21 patients had NPM1 mutations, of whom 20 had a normal karyotype, representing 33% of normal karyotype AML patients. Of these, 10 patients also had FLT3 rearrangements, whereas 20 | haematologica/the hematology journal | 2007; 92(s1) 10 had only NPM1mutations without FLT3 rearrangements. Although our sample is small, our findings were in accordance with the literature: patients with NPM1 mutations had a longer survival than those without such mutations, but only if FLT3 rearrangements were not present. Two thirds of the NPM1 positive patients were female. Our percent of normal karyotype/NPM1 positive patients (33%) is somewhat lower than that reported in the literature [45.7% (Theide, 2006) to 50-60% (Falini, 2006))]. The slightly lower percent could be due to a number of factors, such as the small sample size of our group. Alternatively, it could be due to the younger age of our patient population. The mean age of our patients positive for NPM1 mutations was 46 years (range 17-79) as compared to 48 (17-87) without NPM1 mutations. Falini (2005) reported that the NPM1 positive patients were significantly older (51.8 years) than NPM1 negative patients (41.9 years) (Falini, 2005). Thiede (2006) also reported a slightly older age for NPM1 positive compared to negative patients, in a population whose median age was 60 years. Summary and Conclusions. We conclude that melting temperature DNA-based NPM1 analysis is useful in rapid determination of NPM1 status. Patient age may influence the development of NPM1 mutations. 0055 ARE COMORBIDITY SCORES USEFUL DECISION MAKING TOOLS FOR INTENSIVE CHEMOTHERAPY IN ELDERLY PATIENTS WITH ACUTE MYELOID LEUKEMIA? H. Dombret, 1 J.V. Malfuson, 2 A. Etienne, 3 P. Turlure, 4 T. De Revel, 2 D. Bordessoule, 4 N. Vey, 3 C. Gardin5 1 Hopital Saint-Louis, PARIS; 2 Hopital Percy, CLAMART; 3 IPC, MARSEILLE; 4 CHU, LIMOGES; 5 Hopital Avicenne, BOBIGNY, France Aim. We have recently reported results of standard intensive chemotherapy in 416 patients with AML aged 65 years or more (median, 72 years) treated in the ALFA-9803 trial. We report here on the impact of pretreatment comorbidities on mortality before day 100 (d100 mortality, 22% in the whole patient population) and survival in this large cohort of patients. Methods. For each patient, we calculated the original Charlson Comorbidity Index (CCI) (Charlson, J Chron Dis 1987) and the refined Hematopoietic Cell Transplantation Comorbidity Index (HCT- CI) (Sorror, Blood 2005). Results. As expected, both scores correlated pretty well (CCI 0/1/2=353/57/6; HCTCI 0/1/2/3+ = 268/85/42/21; p1 demarcated only 15% of high-risk patients with a d100 mortality rate of 35% and higher HCTCI levels only 5% of patients or less. In addition, the predicted d100 mortality was 21% in a patient with HCTCI>1 due to cardiac abnormality and/or diabetes and/or obesity versus 47% in a patient with HCTCI=1 due to infection only, indicating that some HCTCI items did not impact on outcome. Further analysis of the prognostic impact of each comorbidity or combination led us to propose only four independent criteria (pre-treatment documented infection, chronic pulmonary disease, PS>1 if age>74y, and high-risk cytogenetics) to consider a patient as unfit for intensive chemotherapy, even if he/she fulfilled all usual inclusion criteria. This 4-criteria non-additive tool was associated with a higher decisional value allowing to demarcate 28% of patients with a d100 mortality rate of 43% and a specificity of 86%. This new definition of unfit patients was validated in a set of patients from one independent French institution.
0056 PROGNOSTIC SIGNIFICANCE OF FLT3/ITD MUTATION IN PATIENTS WITH AML1/ETO ASSOCIATED ACUTE MYELOID LEUKEMIA Y.-K. Kim, 1 H.N. Kim, 2 I.K. Lee, 2 D.Y. Jo, 3 J.H. Won, 4 J.H. Choi, 2 S.R. Lee, 1 H.J. Shim, 1 J. S. Ahn, 1 D.H. Yang, 1 J.J. Lee, 1 H.S. Park, 4 H.J. Kim 1 1 Chonnam National University Hwasun Hosp, JEOLLANAM-DO; 2 GRCHD, Chonnam Natl. Univ. Hwasun Hosp., JEOLLANAM-DO; 3 Chungnam National University Hospital, DAEJEON; 4 Soonchunhyang Univ. College of Med., SEOUL, South-Korea Background. AML1/ETO fusion gene in acute myeloid leukemia (AML) usually predicts a good response to chemotherapy with a high remission rate and a relatively long median survival. An internal tandem duplication of the FLT3 gene (FLT3/ITDs) is known to be associated with poor outcome in AML patients. In these days, animal study showed that the dual presentation of AML1/ETO fusion gene and the FLT3 length mutation collaborate in inducing acute leukemia in mice. Aims. To determine the prognostic role of FLT3/ITD mutation in patients with AML1/ETO positive AML. Methods. FLT3/ITD mutation status was evaluated by performing DNA polymerase chain reaction assays on 38 bone marrow samples obtained at initial diagnosis from the patients with AML1/ETO fusion gene positive AML. GeneScan analysis was performed to confirm the FLT3/ITD mutation and to measure mutant levels. Results. Of total 38 patients, 9 patients (23.7%) demonstrated the aberrant FLT3/ITD mutations. The median age of patients was 37 years (range, 18-75 years). There were 23 males (60.5%) and 15 females (39.5%). There was no statistically significant difference in age, gender, leukocyte count, hemoglobin level, platelet count and percentage of peripheral or bone marrow blasts between the patients with FLT3/ITD and the patients without FLT3/ITD. To analyze the response to or outcome of therapy, we evaluated 33 patients who received intensive induction chemotherapy containing cytarabine. In univariate analysis, there was no significant difference in complete response rate (100% vs. 95.8%, p=0.53). However, the presence of FLT3/ITD was associated with higher relapse rate in these patients (77.8% vs. 30.4%, p
Page 1 and 2: haematologica the hematology journa
Page 3 and 4: Information for readers, authors an
Page 5 and 6: EHA Executive Board E. Hellström-L
Page 7 and 8: Poster session I POSTER SESSION POS
Page 9 and 10: 12 th Congress of the European Hema
Page 11 and 12: dasatinib. Methods. We studied Ikar
Page 13 and 14: Expression of the oncogene H-Ras an
Page 15 and 16: is the gene for the erythropoietin
Page 17 and 18: safety of a slow-release liposomal
Page 19 and 20: 0029 OUTCOME OF THE TREATMENT OF AD
Page 21 and 22: drug-induced apoptotic response of
Page 23 and 24: 41% in the PI3K- group (p=0.001). I
Page 25 and 26: Acute myeloid leukemia - Clinical I
Page 27: to 60 years (n=116, or 72%) receive
Page 31 and 32: Anemia and Bone marrow failure 0061
Page 33 and 34: tified with the current protocol. S
Page 35 and 36: new cases of lead poisoning due to
Page 37 and 38: icance, from baseline to week 6 (p
Page 39 and 40: 0086 THROMBELASTOGRAPHIC CHART RELI
Page 41 and 42: trials. The aim of this retrospecti
Page 43 and 44: tant function in this disease, nega
Page 45 and 46: ed to a favorable outcome. Bialleli
Page 47 and 48: stronger levels of p21 in the cell
Page 49 and 50: hematological centers in one countr
Page 51 and 52: ure 1). Conclusions. Results for re
Page 53 and 54: patients. After a median follow-up
Page 55 and 56: Cytogenetics and Molecular diagnost
Page 57 and 58: 0135 ROUTINE DETECTION OF CYTOGENET
Page 59 and 60: (MMolR, defined as a BCR-ABL x 100
Page 61 and 62: 0146 ARSENIC TRIOXIDE INDUCES ACCUM
Page 63 and 64: tinguish between genotypic B-cell l
Page 65 and 66: Genomics and proteomics 0158 PLASMA
Page 67 and 68: 0164 EVALUATION OF MULTIPLEX LIGATI
Page 69 and 70: each patient’s replicate conditio
Page 71 and 72: 0174 RELATION BETWEEN LOW PML-RARα
Page 73 and 74: 0179 ESHAP VS GIN AS SALVAGE AND MO
Page 75 and 76: Immunology and gene therapy 0184 EA
Page 77 and 78: Cell viability was not affected by
Page 79 and 80:
month is not relevant to chronic Gv
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Infection and supportive care I 020
Page 83 and 84:
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
Page 123 and 124:
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
Page 165 and 166:
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
Page 247 and 248:
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
Page 257 and 258:
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
Page 265 and 266:
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
Page 305 and 306:
0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
Page 309 and 310:
p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
Page 313 and 314:
Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
Page 317 and 318:
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
Page 323 and 324:
0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
Page 329 and 330:
0862 COMPARISON OF DASATINIB TO HIG
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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
Page 341 and 342:
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
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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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
Page 361 and 362:
that the incidence of JAK2 mutation
Page 363 and 364:
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
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
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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
Page 403 and 404:
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
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
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were incidentally diagnosed (52%).
Page 429 and 430:
ß2GP1 may be considered as determi
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characterized in 198 β thalassaemi
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1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
Page 437 and 438:
in age. High prevalence of LBM amon
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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
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admitted to ICU were discharged des
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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
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
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nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
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gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
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Results. Though there was no recogn
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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
Page 505 and 506:
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
Page 513 and 514:
acute leukemia. However, we cannot
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agents. They involve primarily the
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voriconazole for 2 months followed
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typed using a commercially availabl
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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
Page 529 and 530:
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
Page 539 and 540:
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,
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.,
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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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12 th Congress of the European Hema
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12th Congress of the European Hematology ... - Haematologica

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