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12 th Congress of the European Hematology Association used per patient for these analyses. Results. The molecular marker (TCRD- LMO2 breakpoint region, n=1, TCR rearrangement, n=2) was detected in only three of 11 patients 3,3 years old or younger but in none of the older ones. The positivity at birth did not correlate with other clinical or biological features as for example leukemia subtype, presence of a thymus tumor or extent of bone marrow and peripheral blood infiltration. Summary and Conclusions. This is the first comprehensive study performed in children with T ALL to assess the in utero origin of their disease. Our data provide first evidence for a predominant postnatal origin of T ALL in the majority of cases with a rare prenatal initiation only in young children. These data suggest, in line with mouse and zebra fish models for T ALL and the data derived from the T ALL-like disease in two children with retroviral gene transfer for SCID-X1, that T ALL is not only a rapidly proliferating disease when fully malignant, but that the latency, the time from initiation to the clinical manifestation, might also be short. The results are in sharp contrast to B cell precursor ALL in children for whom an in utero initiation was demonstrated not only in the majority of cases with genetically diverse subgroups but also for children, who were older at the clinical manifestation of the leukemia. This work was supported in part by a the Oberösterreichischen Kinderkrebsforschung (KS), the St. Anna Kinderkrebsforschung (SF, RPG) and the Wilhelm Sander-Foundation (MM). 0875 EML1-ABL1 IS ACTIVATED BY COILED COIL MEDIATED OLIGOMERIZATION AND INDUCES T-CELL ACUTE LYMPHOBLASTIC OR CHRONIC MYELOID LEUKEMIA IN A MOUSE BONE MARROW TRANSPLANT MODEL K. De Keersmaecker, 1 H. Verachtert, 1 W. Landuyt, 1 C. De Wolf-Peeters, 1 P. Vandenberghe, 1 J. Schwaller, 2 P. Marynen, 1 J. Cools1 1 2 University of Leuven, LEUVEN, Belgium; University Hospital Basel, BASEL, Switzerland Background.BCR-ABL1 (BCR-ABL) is a potent oncogenic tyrosine kinase that is activated by coiled coil mediated oligomerization and by coiled coil independent mechanisms. BCR-ABL1 is common in CML and B-ALL, but is rarely found in T-ALL. The EML1-ABL1 fusion is a variant ABL1 fusion gene that we identified in a T-ALL patient. Aims. We aimed at comparing the oncogenic properties of BCR-ABL1 and EML1-ABL1 using in vitro and in vivo models. Characterization of ABL1 fusions such as EML1-ABL1 could also provide valuable insights to better understand the oncogenic properties of BCR-ABL1. Methods. We generated BCR- ABL1 and EML1-ABL1 constructs as well as deletion constructs and transduced those to the murine IL-3 dependent Ba/F3 cell line. EML1-ABL1 and EML1-ABL1 deletion variants were assayed for autophosphorylation and for their ability to transform Ba/F3 cells to IL-3 independent growth. Using a mouse bone marrow transplant model, we determined the transforming properties of EML1-ABL1 in vivo. Results. Both BCR- ABL1 and EML1-ABL1 transformed Ba/F3 cells to IL-3 independent growth, although EML1-ABL1 showed weaker autophosphorylation compared to BCR-ABL1. EML1-ABL1 forms homodimers, and deletion of the coiled coil domain of EML1 abrogated its transformation in Ba/F3 cells. These observations suggest that EML1-ABL1, in contrast to BCR- ABL1, only depends on oligomerization for its activation, which may explain the observation of weaker kinase activity of EML1-ABL1. In addition, deletion of part of EML1, resulting in a direct fusion between the EML1 coiled coil domain and ABL1 resulted in increased autophosphorylation. In a murine retroviral bone marrow transplant model, 50% of the mice transplanted with EML1-ABL1 transduced bone marrow cells developed a transplantable fatal T-ALL, characterized by leukocytosis, splenomegaly, and massive infiltration of bone marrow and spleen by CD4 + /CD8 + blast cells. The remaining 50% of recipients of EML1-ABL1 transduced bone marrow cells developed either a non-transplantable CML-like disease (30% of mice) with leukocytosis, splenomegaly, and infiltration of bone marrow and spleen by Mac1 + /Gr1 + maturing granulocytes, or a mixed T-ALL/CML-like disease (20%). All EML1-ABL1 associated diseases had a latency of 96 -119 days, which is significantly longer than the 15-21 days latency associated with BCR-ABL1 induced CMLlike disease. The longer latency for EML1-ABL1 associated disease indicates that the acquisition of additional mutations is required. Some of the mice displayed expression of transcription factors LYL1, TAL1 and LMO2, known to be associated with human T-ALL. Activating NOTCH1 mutations could not be detected. In contrast to EML1-ABL1 induced disease, mice transplanted with the more active deletion variant with the EML1 coiled coil domain fused to ABL1 developed a CML-like disease with much shorter latency (36 days). Conclusions. In contrast to BCR- ABL1 which is activated by coiled coil dependent and independent mechanisms, coiled coil mediated oligomerization is necessary and sufficient 326 | haematologica/the hematology journal | 2007; 92(s1) for EML1-ABL1 kinase activity and transforming properties. Our data suggest that kinase activity of ABL1 fusions may determine in part the disease phenotype. The mouse model we describe for EML1-ABL1 induced T-ALL can be further explored to identify co-operating events in the pathogenesis of T-ALL and for testing novel therapies. 0876 ANALYSIS OF PAIRED PRESENTATION AND RELAPSE SAMPLES IN T-ALL SUGGESTS THAT, AT LEAST IN SOME PATIENTS, NOTCH-1 MUTATIONS MAY BE ACQUIRED AS A SECONDARY EVENT M. Mansour, 1 V. Duke, 2 B. Patel, 2 P. Ancliff, 3 L. Foroni, 2 R.E. Gale, 1 D.C. Linch1 1 University College London, LONDON; 2 Royal Free Hospital, LONDON; 3 Great Ormond Street Hospital, LONDON, United Kingdom Background.Activating mutations in Notch-1 are present in over 50% of patients with T-cell acute lymphoblastic leukaemia (T-ALL). It has been proposed that acquisition of these mutations may be an early event in leukaemogenesis, committing common lymphoid progenitors towards a T-cell fate before the acquisition of other secondary mutations. They may thus represent potential targets for minimal residual disease (MRD) analysis which can be limited, particularly in adults, by the inability to identify suitable and stable gene rearrangements in the T-cell receptor (TCR). Aims. To determine the stability of Notch-1 mutations in paired presentation-relapse samples. Methods. Presence of Notch-1 mutations in the HD-N, HD-C, TAD and PEST domains was investigated in 51 presentation T-ALL samples (34 adults, 17 children) and 14 paired relapse samples using PCR and denaturing HPLC (Transgenomic WAVE ® ). Abnormal chromatograms were sequenced to identify the mutation, with purification of low level mutations where necessary. Relative mutant level was quantified in products with a size difference (insertions or deletions) using fragment analysis (Beckman Coulter CEQ8000). T-cell receptor (TCR) clonality was performed at the TCRα locus using standard techniques. Same patient identity was confirmed in the paired presentation-relapse samples using analysis at 4 short tandem repeat loci. Results. At presentation a total of 49 mutations were detected in 36 patients (70%), 12 of whom had more than one mutation. Seven of the mutations appeared to be low level from the WAVE pattern. Quantification was possible in four of them and confirmed that the relative mutant level was 6-10% of total despite the presence of greater than 85% blasts. Furthermore, 3 of the patients with low level mutations also had a high level mutation in another domain, suggesting the former were acquired as a secondary event in a subclone. Of 14 matched pairs, 7 were wild type at both presentation and relapse. Four of the 7 mutant-positive patients at presentation relapsed with the same mutation(s), with no change in mutant level which was high. Three patients had evidence of a change in mutant at relapse. One patient lost a low-level HD-C mutation but gained a high level HD-N mutation which could not be detected at presentation using mutant-specific qPCR at a sensitivity of 1×10 –4 . The patient had the same two TCR Vα1 clones at both presentation and relapse. Another patient lost a high level PEST mutation at relapse whilst a low level HD-C mutation progressively increased at both first and second relapse (6%, 21% and 33% respectively). The same TCR Vα11 clone was detected at each time point. A third patient lost both a high level HD- N and PEST mutation and gained a different PEST mutation; in this case, the TCR clone at relapse was different, suggestive of a secondary T-ALL. Summary. These data suggest, at least in some cases, Notch-1 mutations post-date the TCR rearrangement and can be acquired as a secondary event. The loss of mutations at relapse in 3 of 7 mutant-positive patients indicates that caution must be exercised in using them as single MRD targets.
0877 PAX5/TEL TRANSDUCED PRE-BI CELLS ARE RESISTANT TO TGF-β1 AND MIGRATE TOWARDS SDF-α G.F. Fazio, 1 C. Palmi, 2 V. Andrè, 2 A Biondi, 2 A. Rolink, 3 G. Cazzaniga 2 1 Tettamanti Reserach Center, MONZA, Italy; 2 Tettamanti Research Center, MONZA, Italy; 3 University of Basel, BASEL, Switzerland Background. PAX5 is a transcription factor essential for B cell development. Recent data indicate that PAX5 aberrancies are present in approximately 30% of pediatric B-cell precursor ALL. We previously cloned the PAX5/TEL chimeric gene, originated from the translocation t(9;12) (q11;p13) in an ALL patient. PAX5/TEL is likely to be an aberrant transcription factor, resulting from joining the 5’ region of PAX5 to the 3’ region of the TEL/ETV6 (Ets-family DNA binding domain) gene. We have demonstrated a specific nuclear localization of the chimeric protein in NIH3T3 by immunofluorescence analysis. Moreover, in IL-3 dependent murine proB Ba/F3 cells, PAX5/TEL recruits mSin3A corepressor, suggesting its function as transcriptional suppressor. Aim of the study was to investigate the functions of the PAX5/TEL chimeric protein in preBI cells purified from mice fetal liver. Methods. murine PAX5 -/- (B220 + /C- KIT + /CD19 – ) and wild type (B220 + /C-KIT + /CD19 + ) preBI cells were transduced with pMIGR-PAX5/TEL-IRES-GFP retroviral construct. Both PAX5- /- preBI cells and wild type preBI cells were cultured on OP9 stromal cells in IMDM +2%FCS and IL-7. Results. PAX5/TEL transduced wild type preBI cells showed down modulation of CD19 and slight increase in c- KIT level expression, while B220 antigen progressively became negative. PAX5 -/- preBI cells transduced with PAX5/TEL did not show any difference with the parental cells. Transwell assay showed increased migration index of PAX5/TEL wt preBI cells towards SDF-1α chemokine, indicating a tendency to migrate into bone marrow. RQ-PCR data indicates that this could be mediated by modulation of CXCR4 receptor levels. Without IL-7, after 24-48 of withdrawal, PAX5/TEL wt preBI cells were still proliferating, while control cells died; although they did not show a complete cytokine independence, after 72-96 hours of starvation, PAX5/TEL cells were still alive, showing an advantage in cell survival. PAX5/TEL cells were resistant to TGF-β1 anti-proliferative and apoptotic effects, continuing to actively proliferate in presence of the cytokine, with a three-fold increased growth rate than control cells. Conclusions. PAX5/TEL showed a role of transcriptional suppressor in wt preBI cells, down regulating CD19 expression; this, in addition to B220 decrease, indicates that PAX5/TEL can drive the regression of preBI cell into a previous B cell differentiation stage, e.g. proB cells. PAX5/TEL do not replace PAX5 functions in PAX5 -/- cells; indeed it cannot activate PAX5 target genes as CD19, important for restoring B cell differentiation potential. Both during the culture without the IL-7 and during the culture in presence of TGF-β1, PAX5/TEL gives proliferation and survival advantage to cells, by offering them a chance to resist to apoptotic stimuli, thus potentially predisposing for further events leading cell transformation. 12 th Congress of the European Hematology Association Thrombosis and bleeding disorders 0878 SOLUBLE P-SELECTIN AND THROMBOSIS RISK OF PATIENTS WITH A PERSISTENT LUPUS ANTICOAGULANT IN A PROSPECTIVE COHORT STUDY R. Vormittag, 1 S. Panzer, 2 C. Ay, 3 P. Quehenberger, 4 S. Koder, 3 I. Pabinger3 1 MUW, VIENNA; 2 Clinic for Blood Group Serology, MUW, VIENNA; 3 Internal Medicine I, MUW, VIENNA; 4 KIMCL, MUW, VIENNA, Austria Background. Increased soluble P-selectin (sP-selectin) was associated with an about 10-fold increased risk of recurrent venous thromboembolism in a case/control study. No prospective data on the thrombosis risk of LA-patients with elevated sP-selectin levels are currently available. Aims. Therefore, it was the aim of our study to assess the value of elevated sP-selectin levels as a predictive parameter for thromboembolic events in LA-patients. Methods. Diagnosis of LA was made according to established criteria. sP-selectin was determined by ELISA (Human soluble P- Selectin Immunoassay, R&D Systems, USA). Elevated sP-selectin was defined as a value exceeding the 95th percentile of control group of 129 individuals (cutoff=55.1 ng/mL). LA-patients were asked to participate in the study at the time of diagnosis of LA or at the time of their first presentation at the outpatient ward if the diagnosis of LA had already been established. After patients had given their informed consent their medical history was recorded and they were followed prospectively. Study endpoints were objectively confirmed arterial or venous thromboembolic events, death or loss of follow-up. The study design was approved by the Ethics Comittee of the Medical University Vienna. Results. Ninety-seven LA-patients were included (80 women, 17 men; median age 42, range 17-86 years). Sixty-nine LA-patients had a history of thrombotic events (59 women, 10 men) and 52 of these (75%) were under oral anticoagulation at the time of study inclusion. Twenty-eight LA-patients (21 women, 7 men) did not have a history of thrombosis and nobody in this group was under oral anticoagulation. sP-selectin levels were significantly higher in LA patients with a history of thrombosis (median 44.1 ng/mL, range 9.8-130.1) than in those without (median 35.5 ng/mL, range 15.6- 74.1, p=0.008). An odds ratio for past thrombosis of 6.5 [95% confidence interval: 1.4-29.8] was calculated for elevated sP-selectin. During followup (median observation time: 911 days, range: 80-1973) ten thrombotic events were observed (four deep vein thromboses, one pulmonary embolism, three strokes and two myocardial infarctions), of these were seven recurrent events in patients with a history of thrombosis and three primary events. Elevated sP-selectin was present in 25 patients (26%). The cummulative probability of thrombosis was 12.2% after one year and 16.8% after five years in patients with elevated sP-selectin, whereas it was 2.8% after one year and 14.5% after five years for LA-patients with sPselectin below the cutoff (Figure 1). Figure 1. Venous and arterial thrombotic events in LA-patients with (continuous line) and without (discontinued line) elevated sP-selecti levels. haematologica/the hematology journal | 2007; 92(s1) | 327
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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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Page 309 and 310: p=0.014 and p=0.003, respectively).
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1018 THE EFFECT OF THE SUGARBAKER P
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1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
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1063 ABNORMAL METHYLATION STATUS OF
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1069 CLINICAL RELEVANCE OF REGULATO
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1076 SERUM LEVELS OF SOLUBLE HLA CL
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patient is still undergoing intensi
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nificant MVD differences were detec
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dictor of OS (p=0.004). High dose t
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1099 ALTERATIONS IN THE NATURAL KIL
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1105 CYTOGENETIC ABNORMALITIES IN 3
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1110 CONSTITUTIVE ACTIVATION OF STA
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efficacy results with a well-tolera
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unmutated VH genes, and high and lo
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Aims. Aim of this study was to pred
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tested across a wide range of human
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were incidentally diagnosed (52%).
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ß2GP1 may be considered as determi
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characterized in 198 β thalassaemi
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1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
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of the drug is crucial to allow lon
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egarding cost analysis of ASCT in G
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ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
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events -Postoperative states: 9,19%
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efficacy and decreased atherosclero
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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
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
Page 497 and 498:
Results. Though there was no recogn
Page 499 and 500:
2% and 19% of patients with or with
Page 501 and 502:
were older than 65 y) which can be
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
Page 505 and 506:
median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
Page 509 and 510:
to the presence of IVS1-6 mutation
Page 511 and 512:
fy predictive factors for these abn
Page 513 and 514:
acute leukemia. However, we cannot
Page 515 and 516:
agents. They involve primarily the
Page 517 and 518:
voriconazole for 2 months followed
Page 519 and 520:
typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
Page 523 and 524:
with development of BC/AP. 2. EVI-1
Page 525 and 526:
1447 THE IMPACT OF DISPARITY IN SHO
Page 527 and 528:
three had visual field defects, two
Page 529 and 530:
acquired mutation most prone to cau
Page 531 and 532:
1466 ROS GENERATION AND APOPTOSIS I
Page 533 and 534:
1473 DIARRHEIC SYNDROME, A CLINICAL
Page 535 and 536:
gene fusion is an independent progn
Page 537 and 538:
1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
Page 541 and 542:
immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
Page 545 and 546:
Hodgkin’s disease is well known,
Page 547 and 548:
gram provided a unique chance to de
Page 549 and 550:
even when ADP-induced plt activatio
Page 551 and 552:
medullary involvement of multiple m
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
Page 555 and 556:
1548 QUALITY ANALYSIS OF THE MULTID
Page 557 and 558:
Index of authors A Aapro, M., 0377,
Page 559 and 560:
Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
Page 567 and 568:
El-Sharkawy, N., 0016 Elwahidi, G.,
Page 569 and 570:
Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
Page 573 and 574:
Jaksic, B., 0127, 0446 Jaksic, O.,
Page 575 and 576:
Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
Page 581 and 582:
Musto, P., 0254, 0401, 0422, 0569,
Page 583 and 584:
Papadavid, E., 1442 Papageorgiou, E
Page 585 and 586:
Probatova, N., 0704 Prochazka, V.,
Page 587 and 588:
Rykavicin, O., 0504 Ryningen, A., 0
Page 589 and 590:
Sirard, C., 0127, 0128 Sirigou, A.,
Page 591 and 592:
Thiebaut, A., 0454 Thieblemont, C.,
Page 593 and 594:
Vincenzi, C., 1060 Viniou, N.-A., 0
Page 595 and 596:
Zouabi, H., 0503, 0999 Zoumbos, N.C
Page 597 and 598:
Page 599 and 600:
Page 601 and 602:
Page 603:
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