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12 th Congress of the European Hematology Association ues whereas 18 (52,9%) revealed a positive value for CRAC. This distribution is comparable to the pattern found in the analysis of acute lymphoblastic leukemia in our previous study (N=78, CRAC positive n=35, 44,9%; CRAC negative n=43, 55,1%). Conclusions. The analysis of cytochrome c related caspase activation (CRAC) identifies leukemia samples with deficient apoptosis signaling in a group of pediatric AML patients. The detection of such patients by assessment of the parameter CRAC may be used for additional treatment stratification in childhood acute myeloid leukemia. This work is supported by an EHA research fellowship grant to L.H. Meyer. 0473 FLT-1 ACTIVATION BY VEGF/PLGF INDUCES LEUKEMIA CELL MIGRATION VIA P38/ERK1/2 KINASE PATHWAY, RESULTING IN RHO GTPASES ACTIVATION AND CAVEOLAE FORMATION C. Casalou, R. Fragoso, J.F. Nunes, S. Dias Portuguese Institute of Oncology, LISBON, Portugal Vascular endothelial growth factor (VEGF) receptors -1 (FLT-1) and - 2 (KDR) are expressed by subsets of malignant hematopoietic cells, where they signal in a paracrine and/or autocrine manner to induce cell survival, proliferation and migration. We recently demonstrated that acute lymphoblastic leukemia (ALL) migration in response to VEGF via FLT-1 modulates the onset of extramedulary disease, and thus has clinically predictive value. However the molecular mechanisms involved in leukaemia cell migration were not yet characterized and are the subject of this study. We demonstrate that FLT-1 activation by VEGF or PLGF stimulation results in a significant increase of AML migration, having a minor proliferative effect. This FLT-1 mediated migration of AML cells resulted in the formation of actin membrane protrusions (as assessed by phalloidin/FLT-1 immuno-staining and confocal microscopy) with concomitant increased ERK1/2 and P38 phosphorylation and activation of Rho-GTPases and PAK/Cofilin. Also, by immunoprecipitation studies, we have shown that PLGF promoted the recruitment of Hsp90 and its binding to FLT-1, actin and caveolin-1. While PLGF stimulation of AML cells induced the formation of caveolae-like structures, cytochalasin D treatment, used as control to block cell migration, was shown to block the molecular interactions between FLT-1, actin, Hsp90 and caveolin- 1.Taken together, these data highlight some of the molecular mechanisms whereby VEGF/PLGF stimulation of FLT-1 on AML cells results in cell migration. As such, our data reveal important biological and mechanistic outputs that may be used to monitor leukemia responses to cytoskeleton-disrupting agents or anti-angiogenic therapies. Our ongoing studies are know focusing on a screening of kinases/phosphatases that affect VEGF production in acute leukemia cells, using a system of retrovirus-based vectors that achieve with high-efficient siRNA-dependent silencing in leukaemia cells. 0474 A RECURRENT IN-FRAME INSERTION IN CEBPA TAD2 REGION IS A POLYMORPHISM THAT DOESNT HAVE A PRONOSTIC VALUE IN AML. A STUDY FROM THE FRENCH ALFA GROUP V. Biggio, 1 A. Renneville, 2 O. Nibourel, 2 N. Philippe, 2 L. Terriou, 2 C. Roumier, 2 P. Amoyuel, 3 D. Cottel, 3 D. Cottel, 3 S. Castaigne, 4 H. Dombret, 5 X. Thomas, 6 C. Preudhomme2 1 INSERM, LILLE; 2 INSERM U837, Lab of Hemat. CHRU, LILLE; 3 INSERM U744, INSTITUT PASTEUR, LILLE; 4 Dep of Hem., Hôpital André Mignot, VERSAILLES; 5 Dep of Hem. Hôpital Saint-Louis, PARIS; 6 Dep of Hem. Hôpital Edouard Herriot, LYON, France Background. CCAAT/enhancer-binding protein-α (CEBPa) is a transcription factor strongly implicated in myelopoiesis through control of proliferation and differentiation of myeloid progenitors. In patients with acute myeloid leukemia (AML), this gene is often mutated (about 8%). Those mutations are in-frame or out of frame types and the consequences are a loss of function of CEBPa. Among those mutations, an inframe insertion of 6bp in the TAD2 domain, resulting in a His-Pro duplication (HP196-197ins), was found in patients at diagnosis and remission time, letting think of a constitutive abnormality, that may induce AML susceptibility. Surprisingly this 6bp insertion was observed in healthy voluntaries too. Recently Delwel et al. have described this insertion as being a polymorphism. They report that 6bp insertion frequency in AML patients is between 3.2% (9/282) and 3.9% (12/305), while in non-leukemic blood samples, the frequency is 8% (22/274). Further, they didn’t found any correlation with CEBPa gene expression signature 176 | haematologica/the hematology journal | 2007; 92(s1) and more, patients with insertion didn’t show any particular expression profile. Aim of study and Methods. In our study we have investigated 325 AML patients enrolled in ALFA 98-02 protocol and 994 healthy voluntaries for the presence of this insertion by nucleotide sequencing, and we studied its prognostic value. Results. First, we looked for the frequency of this insertion between the healthy whole population and the AML cohort; we didn’t found any difference between AML patients and healthy voluntaries: 6.5% (21/325) versus 6.6% (66/994) respectively. This data strongly suggest that this insertion is a polymorphism, but familiar molecular study should be performed to confirm this hypothesis. Second, we made a comparison between true mutation of CEBPa and this 6bp polymorphism. Patients who harbored only the polymorphism have heterogeneous cytogenetic finding (8 normal, 5 complex and 1 intermediate karyotypes, 4 CBF-AML and 4 unknown), while patients with a true abnormality of CEBPa gene (n=23) show significant association to normal karyotypes (p=0.03). Mutations of CEBPa are often associated to M1 and M2 FAB subtypes, but we didn’t find an association to FAB subtype for the group of patients with 6bp polymorphism. Regarding other molecular prognostic factors, CEBPa is rarely associated to NPM mutations (p=0.03) while polymorphism doesn’t show this particularity (p>0.2). Regarding the EFS, we didn’t find any correlation between this polymorphism, true CEBPa mutations and others patients. However regarding the OS only the true CEBPa mutation patients presented a trend for longer survival. Conclusions. In conclusion, we confirm that HP196-197ins is a common polymorphism spread in normal population and AML patients, without any prognostic value in our cohort of AML patients. 0475 CAN HYPERACTIVE SIGNALLING THROUGH THE RAS PROTEINS INDUCE AML IN MICE? A. Cutts, A.M. Wahlstrom, C. Karlsson, B. Swolin, M.O. Bergo Sahlgrenska University Hospital, GÖTEBORG, Sweden Background. Mutationally activated forms of the RAS proteins, especially the N and K isoforms, are implicated in the pathogenesis of several haematological malignancies, including acute myeloid leukaemia (AML). However, in AML, the mutations in RAS genes are always accompanied by other genetic abnormalities (e.g. MDR1). In mice, hyperactive signalling through the RAS proteins, e.g., via expression of endogenous oncogenic K-RAS or inactivation of the tumor suppressor NF1, results in myeloproliferative disorders (MPD). At this point, it is unclear if hyperactive RAS signalling can induce AML in the absence of other genetic abnormalities. Aims. To test the hypothesis that hyperactive signalling through the RAS proteins can induce AML in mice, without other genetic abnormalities. To accomplish this, we will determine if inactivation of Nf1 - which increases signalling through the N- and K- RAS proteins - will transform a K-RAS-induced MPD into AML. Methods. For these studies, we use Cre-loxP techniques in mice. Cre-induced activation of endogenous oncogenic K-RAS in bone marrow cells results in a rapidly progressing MPD with leukocytosis, splenomegaly, and tissue infiltration; without an increase in blasts in peripheral blood. Similarly, Cre-induced inactivation of the RAS-GAP NF1 results in increased levels of RAS-GTP, hyperactive RAS signalling, and a slowly progressing MPD; without an increase in blasts. In this study, we simultaneously activate the expression of oncogenic K-RAS and inactivate the tumour suppressor NF1 in myeloid cells. This approach allows us to determine if higher levels of RAS-GTP would result in transformation of MPD into AML with > 20% blasts in peripheral blood. Results and Conclusions. This is an ongoing project. By June, 2007, we will have all the necessary data that will allow us to accept or reject our hypothesis. 0476 INCREASED RISK AND EARLY ONSET OF ACUTE MYELOID LEUKAEMIA IN BRAZILIAN INDIVIDUALS WITH NAD(P)H:QUINONE OXIDOREDUCTASE 1 (NQO1) AND CYTOCHROME P450 A1 (CYP1A1) GENE DEFECTS G.G. Yamaguti State University of Campinas (UNICAMP), CAMPINAS, Brazil Background. Acute myeloid leukaemia (AML) has been linked to chronic exposure to benzene and tobacco’s polycyclic aromatic hydrocarbons (PAH). NAD(P)H:quinone oxidoreductase 1 (NQO1) is an enzyme that detoxifies benzene-derived quinones and reduces oxidative stress on hematopoietic cells. A C-->T substitution polymorphism at nucleotide 609 of the NQO1 gene has been linked to a decreased activity of the coded enzyme. On the other hand, PAH are bioactivated by the cytochrome P450 A1 (CYP1A1) enzyme. An A-->G substitution
polymorphism at nucleotide 4889 of the CYP1A1 gene leads to the production of an enzyme with increased activity in PAH metabolism. Moreover, environmental-related diseases resulting from exposure to benzene and tobacco-related diseases have been described as serious health problems in south-eastern Brazil. Aims. The aim of this study was to evaluate the influence of the NQO1 C609T and CYP1A1 A4889G polymorphisms for AML risk and its clinical manifestations in individuals of the south eastern region of Brazil. Methods. Genomic DNA from 133 AML patients and 133 age, gender and race-matched controls were analysed using the polymerase chain reaction (PCR) and enzymatic digestion. The differences between the groups were calculated by the chi-square or Fischer exact test. Results. Controls samples (X 2 =3.69, p=0.07) but not patients samples (X 2 =6.52, 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
Page 133 and 134: Conclusions. This study demonstrate
Page 135 and 136: 0354 FACTOR V LEIDEN HOMOZYGOUS GEN
Page 137 and 138: Results. From July 2005 through Mar
Page 139 and 140: 0364 CLINICAL EFFICACY OF OXALIPLAT
Page 141 and 142: one marrow and peripheral blood ste
Page 143 and 144: ecently suggested (Boissel et al.,
Page 145 and 146: 0378 SAFETY AND EFFICACY OF THE TER
Page 147 and 148: Cytogenetics and molecular diagnost
Page 149 and 150: 0385 CYTOPLASMIC MUTATED NUCLEOPHOS
Page 151 and 152: 0390 ELTROMBOPAG RAISES PLATELET CO
Page 153 and 154: factor for the achievement of CR wa
Page 155 and 156: The cases of RAS showed two peaks o
Page 157 and 158: is 85%. Seven out of the 25 relapse
Page 159 and 160: 0409 FRACTIONATED RADIOIMMUNOTHERAP
Page 161 and 162: 0414 COMPARATIVE ANALYSIS OF THE CO
Page 163 and 164: successfully managed with GM-CSF di
Page 165 and 166: 49% for PCR positive patients (95%
Page 167 and 168: +8 (1 PR+1 HI) and 14/24 pts with c
Page 169 and 170: (e.g. bcr-abl leading to CML). CSC
Page 171 and 172: 0438 TERC MUTATIONS ANALYSIS IN PAT
Page 173 and 174: observed in all mice. Analysis of l
Page 175 and 176: ex-vivo expansion of HUCB-derived H
Page 177 and 178: ic kidney disease in univariate or
Page 179 and 180: One hundred eleven CN AML patients,
Page 181 and 182: to asses intestinal epithelial dama
Page 183: genesis of acute myeloid leukaemia
Page 187 and 188: expression along with a decreased C
Page 189 and 190: 0487 MUTATIONAL STATUS OF NUCLEOPHO
Page 191 and 192: previously reported, a single cours
Page 193 and 194: 0497 SINGLE AGENT CLORETAZINE (VNP4
Page 195 and 196: ly received melphalan-based chemoth
Page 197 and 198: were similar among the 3 groups. Ho
Page 199 and 200: Methods. Several read-out systems w
Page 201 and 202: 0518 SERUM AND CELLULAR EXPRESSION
Page 203 and 204: 0523 DNA REPAIR INHIBITION IN RESTO
Page 205 and 206: held true when BMI-1 expression was
Page 207 and 208: Ph + cells in the bone marrow). We
Page 209 and 210: derivative chromosome (4p16, 7p14,
Page 211 and 212: 0545 STABILIZED BONE MARROW IS NOT
Page 213 and 214: obtained in low (Sokal) risk patien
Page 215 and 216: median dose intensity being 800 (21
Page 217 and 218: from pivotal clinical trials. Metho
Page 219 and 220: Cytogenetics and Molecular diagnost
Page 221 and 222: to set up and optimize a D-HPLC-bas
Page 223 and 224: 0576 WESTERN BLOT IDENTIFICATION OF
Page 225 and 226: Basic disease was AML (n=5), ALL (n
Page 227 and 228: 0588 EXTRACORPOREAL PHOTOPHORESIS F
Page 229 and 230: acquire a cytolytic capacity agains
Page 231 and 232: informed vignettes describing healt
Page 233 and 234: using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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patients had died of their underlyi
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scripts and proteins most affected
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modulated after 24 h (37 up- and 59
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0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
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Results. A total of 396 patients we
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C30 questionnaire, and the correspo
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wave length of light of reflected r
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0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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BRIC 126 and 4N1K) in cells lacking
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sclerosis[NS] and 12 Mixed cellular
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0927 MK-0457, A NOVEL MULTIKINASE I
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Publication Only 0933 CLINICAL FEAT
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HSCT from the available Asian as we
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that the incidence of JAK2 mutation
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without type 2 diabetes. Methods. T
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pts (38.8%) that were isolated (abs
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y using the Miltenyi CD34 isolation
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0969 COMPARISON OF CD25 IMMUNOHISTO
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cytes was 24 days (range 8-32 days)
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a cytogenetic hallmark for M4/M5 su
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normal human BM B progenitor cells
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0994 INCIDENCE OF INVASIVE ASPERGIL
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3 of disease relapse.TRM at day+100
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survival of five years. This dismal
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1011 FLOW CYTOMETRIC DNA INDEX AND
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1018 THE EFFECT OF THE SUGARBAKER P
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1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
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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%
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
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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
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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
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
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median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
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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
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agents. They involve primarily the
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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
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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
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1492 FREQUENCY OF MEDITERRANEAN GLU
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immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
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Hodgkin’s disease is well known,
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gram provided a unique chance to de
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even when ADP-induced plt activatio
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medullary involvement of multiple m
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1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
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Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
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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12th Congress of the European Hematology ... - Haematologica

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