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12 th Congress of the European Hematology Association 0248 COMPARISON OF WHOLE BLOOD VS PURIFIED BLOOD GRANULOCYTES FOR THE DETECTION AND QUANTITATION OF JAK2-V617F E. Hermouet, 1 S. Hermouet, 2 I. Dobo, 3 E. Lippert, 4 M.-C. Boursier, 2 L. Ergand, 2 F. Perrault-Hu, 2 D. Pineau 2 1 Laboratoire d'Hematologie, NANTES; 2 Laboratoire d'Hematologie, CHU Nantes, NANTES; 3 Laboratoire d'Hematologie, CHU Angers, ANGERS; 4 Laboratoire d'Hematologie, CHU Bordeaux, BORDEAUX, France Background. Detection of the V617F mutation of JAK2 (JAK2-V617F) is now one of the first tests performed in the diagnostic work-up of polycythemia and thrombocytoses. When studied in purified blood granulocytes, the JAK2-V617F allelic ratio is typically >20% in Polycythemia vera (PV) but
0250 INACTIVATION OF SUPPRESSOR OF CYTOKINE SIGNALING-1 AND -3 (SOCS-1 AND -3) AND SH2-CONTAINING PHOSPHATASE-1 (SHP-1) IN PHILADELPHIA-NEGATIVE CHRONIC MYELOPROLIFERATIVE DISORDERS (CMPD) M. Lunghi, D. Rossi, C. Deambrogi, M. Cerri, S. Rasi, S. Franceschetti, A. Conconi, P. Riccomagno, D. Capello, G. Gaidano Division of Hematology, NOVARA, Italy Background. Ph-negative chronic myeloproliferative disorders (CMPD) are a clinically overlapping group of disorders characterized by somatic point mutations of the JAK2 gene, leading to constitutive JAK-STAT activation. The negative regulators of cytokine signaling SOCS-1, SOCS-3 and SHP-1 have a crucial function in the down-regulation of JAK-STAT activation in response to cytokines. SHP-1, SOCS-1 and SOCS-3 may be silenced by aberrant DNA methylation and/or mutation in human malignancies. Aims. To test epigenetic and genetic inactivation of SOCS-1, SOCS-3 and SHP-1 in CMPD and acute myeloid leukaemia (AML). Methods. The study was based on: i) 112 CMPD, including 43 essential thrombocythemia (ET), 28 polycythemia vera (PV), 24 idiopathic myelofibrosis in pre-fibrotic phase (MF), 11 atypical chronic myeloid leukemia (ACML), and 6 chronic myelomonocytic leukemia (CMML); ii) 20 AML post-CMPD, including 10 AML from ET, 5 AML from PV and 5 AML from MF. For comparison, 20 normal bone marrow samples were also investigated. All cases were analysed for SOCS-1, SOCS-3 and SHP- 1 aberrant methylation by methylation-specific PCR and for JAK2V617F mutation status by allele specific PCR. SOCS-1 and SOCS-3 mRNA levels were detected by real-time RT-PCR. Mutation of SOCS-1 and SOCS- 3 were tested by DNA direct sequencing. Results. SOCS-3 aberrant methylation occurred with high frequency both in CMPD (46/112, 41%) and in AML post-CMPD (10/17; 59%), and was distributed throughout the different WHO categories: 20/43 (46%) ET, 13/28 (46%) PV, 5/24 (21%) MF, 5/11 (45%) ACML and 3/6 (50%) CMML. Methylation of SOCS-1 and SHP-1 occurred with lower frequency both in CMPD (14/112, 12.5% for SOCS-1; 8/112, 7% for SHP-1) and in AML post- CMPD (3/20, 15% for SOCS-1; 1/20, 5% for SHP-1). In particular, SOCS- 1 methylation was detected in 5/43 (12%) ET, 5/28 (18%) PV, 3/24 (12.5%) MF, 1/11 (9%) ACML, 0/6 CMML. SHP-1 methylation was observed in 4/43 (9%) ET and 4/28 (14%) PV, while it was absent in MF, ACML and CMML. All normal bone marrow samples (n=20) scored negative for SOCS-1, SOCS-3 and SHP-1 methylation. JAK2V617F mutation was detected in 66/112 (59%) Ph-CMPD, including 24/43 (56%) ET, 23/28 (82%) PV, 19/24 (79%) MF, and in 5/20 (25%) AML post- CMPD. SOCS-3, SOCS-1 and SHP-1 methylation occurred in both JAK2V617F-positive (26/66, 39% for SOCS-3; 11/66, 17% for SOCS-1, 6/66, 9% for SHP-1) and JAK2V617F-negative CMPD (12/46, 26% for SOCS-3; 2/46, 4% for SOCS-1, 2/46, 4% for SHP-1). This pattern of SOCS-3, SOCS-1 and SHP-1 methylation was conserved also when the analysis was restricted to PV, ET and MF each as a single group and after stratification for JAK2V617F mutation. By combining the results of SHP- 1, SOCS-1 and SOCS-3 methylation status, 29/66 (44%) JAK2V617F mutated cases carried SHP-1 and/or SOCS-1 and/or SOCS-3 methylation as opposed to 29/46 (43%) germline cases. Similar results were obtained in JAK2V617F-positive and JAK2V617F-negative AML post-CMPD. To verify the correlation between aberrant methylation and gene expression, we analyzed SOCS-3 and SOCS-1 mRNA levels by real-time RT- PCR. SOCS-3 mRNA levels were significantly higher in unmethylated samples (n=10) compared to methylated samples (n=6; p=0.005) and to normal bone marrow (n=10; p=0.03). Similar results were obtained for SOCS-1. SOCS-1 and SOCS-3 missence mutations were detected in 2/104 (2%) and 1/93 (1%) CMPD, respectively. Conclusions. i) Inactivation by aberrant methylation of SOCS-3, SOCS-1 and SHP-1 is involved in the pathogenesis of CMPD, is selectively associated with neoplastic hemopoiesis and correlates with reduced gene expression; ii) methylation of SOCS-3, SOCS-1 and SHP-1 occurs in both JAK2V617F positive and negative cases; iii) the methylation rate of SOCS-3, SOCS-1, and SHP-1 is similar in CMPD and in AML post-CMPD, suggesting that SOCS-3, SOCS-1 and SHP-1 silencing is not involved in leukemic transformation; iv) SOCS-1 and SOCS-3 mutations are rarely involved in CMPD. 12 th Congress of the European Hematology Association 0251 CHARACTERIZATION OF DIFFERENTIALLY EXPRESSED MICRORNAS IN GRANULOCYTES FROM PRIMARY MYELOFIBROSIS P. Guglielmelli, 1 A. Pancrazzi, 1 C. Bogani, 1 L. Tozzi, 1 R. Zini, 2 A. Bosi, 1 R. Manfredini, 2 A.M. Vannucchi1 1 2 Florence University, FLORENCE; University of Modena and Reggio Emilia, MODENA, Italy Background. Despite advances in defining diagnostic and prognostic criteria in patients with Primary Myelofibrosis (PMF), and the recent description of Val617Phe mutation in JAK2 exon12 and of MPL W515K/L mutation, the molecular defect(s) associated with the development of PMF remain still largely to be defined. Comparative transcriptome microarray analysis has allowed us to evidentiate a complex pattern of aberrantly regulated genes in PMF. The underlying mechanism is still poorly understood, but microRNAs might be supposed to play a role in abnormal gene regulation. AIMS. As an approach to identify possibly aberrantly regulated microRNAs in PMF, we used a Human Panel including 150 individual miRNA assays. We performed a comprehensive transcriptome comparative microRNA analysis of normal and PMF granulocytes. METHODS. To this purpose, we prepared four pools, each comprising three subjects, of granulocytes from PMF subjects, two from JAK2V617F wild-type (WT) and two from homozygote patients; two pools from blood donors were used as controls. The method uses stemlooped primers for reverse transcription (RT) of the miRNA, followed by quantitative real-time PCR. The cDNA was analysed with the aid of a TaqMan MicroRNA Assay Human Panel Kit (Applied Biosystem). Results. Ninety six differentially expressed microRNAs were identified; 87 were decreased and 9 were increased. In order to validate these data, we have selected 7 miRNAs which were extremely aberrantly regulated in PMF and we performed a Real-time PCR (RT-PCR) using single TaqMan MicroRNA Assay (Applied Biosystem); these were carried out in an indipendent cohort of normal controls and patients with PMF, polycythemia vera (PV), essential thrombocythemia (ET) and idiopathic erytrocytosis (IE). Three of these gene (miR-150, miR-95 and miR-183) allowed to discriminate patients with PMF from both healthy subjects, IE and others chronic myeloproliferative disorders. We found no difference in expression profile between WT and JAK2V617F homozygote patients. With the aim to confirm the biological effects of these microR- NAs, we have combined miRNA expression data with previously described transcriptosome of CD34 + PMF using microarray analysis (Guglielmelli et al, Stem Cells, 2007:165-73). After identified a number of predicted miRNA 'Targets, we have measured gene expression levels in granulocytes by RT-PCR. We found that MYB, MYCN, LEPR and PRAME were significantly increased in PMF compared with healthy controls as expected for the low levels of miR-150 and miR-183; on the other hand, both DTR and FOSB, and their putative regulatory miR-95 and miR-31, were found concurrently decreased. Conclusions. Recent studies have implicated miRNAs in a number of fundamental cell processes and in hematopoiesis. These data show an unique expression profiling of PMF patients as compared to normal controls, with an observed overall miRNA downregulation, as reported in other cancer cells. Moreover, 3 miRNAs were identified as a predictive signature of PMF as opposed to other myeloproliferative disorders. Finally, we showed correlation between some microRNAs and abnormally regulated putative target genes, suggesting their possible role in disease pathogenesis. haematologica/the hematology journal | 2007; 92(s1) | 91
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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
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
Page 81 and 82: Infection and supportive care I 020
Page 83 and 84: 0206 POTENTIAL ROLE OF CMV IN THE O
Page 85 and 86: 3H-thymidine uptake in cell culture
Page 87 and 88: 0217 TUBERCULOSIS AMONG A COHORT OF
Page 89 and 90: 0222 COMPARISON OF IWG 2006 AND IWG
Page 91 and 92: tem (IPSS) to h-MDS was also invest
Page 93 and 94: PCH97-19) were studied. Conventiona
Page 95 and 96: of erythroid colonies was reduced i
Page 97: 0245 POTENT AND SELECTIVE INHIBITIO
Page 101 and 102: Bortezomib 1.3 mg/m 2 days 1,4,8,11
Page 103 and 104: Response was defined according to E
Page 105 and 106: G-CSF can be used in neutropenic pa
Page 107 and 108: ence and functional activity of CD8
Page 109 and 110: itating tumor development, or engag
Page 111 and 112: phoma and SNT-13, -15 were establis
Page 113 and 114: usage (2/20 ie 10%) were observed.
Page 115 and 116: 0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
Page 117 and 118: (range, 1-6) and 11 treatment cycle
Page 119 and 120: 0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
Page 121 and 122: functional activity was confirmed b
Page 123 and 124: No major toxicity, neither hematolo
Page 125 and 126: enewal potential of X-RAR-positive
Page 127 and 128: (50-99) respectively. Serial analys
Page 129 and 130: cell-interaction, adhesion and acti
Page 131 and 132: 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
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0385 CYTOPLASMIC MUTATED NUCLEOPHOS
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0390 ELTROMBOPAG RAISES PLATELET CO
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factor for the achievement of CR wa
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The cases of RAS showed two peaks o
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is 85%. Seven out of the 25 relapse
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0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
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successfully managed with GM-CSF di
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49% for PCR positive patients (95%
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+8 (1 PR+1 HI) and 14/24 pts with c
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(e.g. bcr-abl leading to CML). CSC
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0438 TERC MUTATIONS ANALYSIS IN PAT
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observed in all mice. Analysis of l
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ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
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One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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genesis of acute myeloid leukaemia
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polymorphism at nucleotide 4889 of
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expression along with a decreased C
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0487 MUTATIONAL STATUS OF NUCLEOPHO
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previously reported, a single cours
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0497 SINGLE AGENT CLORETAZINE (VNP4
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ly received melphalan-based chemoth
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were similar among the 3 groups. Ho
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Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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0523 DNA REPAIR INHIBITION IN RESTO
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held true when BMI-1 expression was
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Ph + cells in the bone marrow). We
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derivative chromosome (4p16, 7p14,
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0545 STABILIZED BONE MARROW IS NOT
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obtained in low (Sokal) risk patien
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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patients had died of their underlyi
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scripts and proteins most affected
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modulated after 24 h (37 up- and 59
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0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
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Results. A total of 396 patients we
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C30 questionnaire, and the correspo
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wave length of light of reflected r
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0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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BRIC 126 and 4N1K) in cells lacking
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sclerosis[NS] and 12 Mixed cellular
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0927 MK-0457, A NOVEL MULTIKINASE I
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Publication Only 0933 CLINICAL FEAT
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HSCT from the available Asian as we
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that the incidence of JAK2 mutation
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without type 2 diabetes. Methods. T
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pts (38.8%) that were isolated (abs
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y using the Miltenyi CD34 isolation
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0969 COMPARISON OF CD25 IMMUNOHISTO
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cytes was 24 days (range 8-32 days)
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a cytogenetic hallmark for M4/M5 su
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normal human BM B progenitor cells
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0994 INCIDENCE OF INVASIVE ASPERGIL
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3 of disease relapse.TRM at day+100
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survival of five years. This dismal
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1011 FLOW CYTOMETRIC DNA INDEX AND
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1018 THE EFFECT OF THE SUGARBAKER P
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1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
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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
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
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ly express the cytoplasmic (inactiv
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findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
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phamide 750 mg/m 2 on day 1, vincri
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nomenon is unclear. It has been sug
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oped mild thrombocytopenia (platele
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gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
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(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
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typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
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with development of BC/AP. 2. EVI-1
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1447 THE IMPACT OF DISPARITY IN SHO
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three had visual field defects, two
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acquired mutation most prone to cau
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1466 ROS GENERATION AND APOPTOSIS I
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1473 DIARRHEIC SYNDROME, A CLINICAL
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gene fusion is an independent progn
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1484 EPIDEMIOLOGY AND RESPONSE TO T
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1492 FREQUENCY OF MEDITERRANEAN GLU
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immune globulin was administered at
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maintained on Imatinib 400 mg. Afte
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Hodgkin’s disease is well known,
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gram provided a unique chance to de
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even when ADP-induced plt activatio
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medullary involvement of multiple m
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1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
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Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
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.,
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Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
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Musto, P., 0254, 0401, 0422, 0569,
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Papadavid, E., 1442 Papageorgiou, E
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Probatova, N., 0704 Prochazka, V.,
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Rykavicin, O., 0504 Ryningen, A., 0
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Sirard, C., 0127, 0128 Sirigou, A.,
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Thiebaut, A., 0454 Thieblemont, C.,
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Vincenzi, C., 1060 Viniou, N.-A., 0
Page 595 and 596:
Zouabi, H., 0503, 0999 Zoumbos, N.C
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12th Congress of the European Hematology ... - Haematologica

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