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12 th Congress of the European Hematology Association 0009 REFINEMENT OF THE REGIONS OF MINIMAL DELETION AT 6Q IN CHILDHOOD T-ALL BY BAC TILING PATH ARRAY CGH M.P. Pisecker, 1 F. Erdogan, 2 R. Ullmann, 2 G. Mann, 1 S. Strehl1 1 CCRI, Children´s Cancer Research Inst., VIENNA, Austria, 2 Max Planck Inst. for Molecular Genetics, BERLIN, Germany Background. T-cell acute lymphoblastic leukemia (T-ALL) is a highrisk malignancy of thymocytes, and accounts for 10-15% of pediatric ALL cases. In T-ALL genetic analyses have elucidated an enormous heterogeneity in genetic abnormalities including chromosomal translocations, deletions, amplifications, and mutations. In particular, quantitative changes seem to play a crucial role in the pathogenesis and progression of the disease. Among these, deletions of the long arm of chromosome 6 have been found in 10-15% pediatric T-ALL. However, owing to the heterogeneity in the extent and the location of the 6q deletions, only one potential tumor suppressor gene, GRIK2, contributing to the pathogenesis of T-ALL has yet been identified in this region. Aim and Methods. This study was aimed at the refinement of the regions of minimal deletion (RMD) at 6q in childhood T-ALL by means of BAC tiling path array comparative genomic hybridization (CGH) with the final goal to identify novel genes possibly implicated in the development or progression of T-ALL. Results. Genomic DNAs extracted from 70 diagnostic bone marrow samples of childhood T-ALL patients were subjected to BAC tiling path array CGH. In 7 (10%) of the cases a del(6q) was detected, which is in accordance with formerly published incidences. Comprehensive data analysis allowed to determine two different potential RMDs on chromosome 6q14.1-15 and 6q16.2 corroborating the notion that not all cases with a del(6q) share a common RMD. The RMD at 6q14.1- 15, which encompassed approximately 12 Mb was deleted in 6 of the cases, and apart from several other genes contained the previously described putative tumor suppressor gene GRIK2. The second, much smaller potential RMD at 6q16.2, spanned roughly 270 kb, and was also consistent with a common deleted region in 6 of the cases. This MRD contained only two genes, namely POU3F2 and FBXL4. POU3F2 (homeobox/POU domain protein 2) is a transcription factor, which is mainly expressed in fetal brain and melanocytes, and its expression is known to be altered in melanoma. The second gene, FBXL4, encodes a protein, which is a member of the F-box protein family and is probably involved in the phosphorylation-dependent ubiquitination of proteins, has so far not been shown to be implicated in any type of cancer. Conclusions. Analysis of hematopoietic diseases by BAC tiling path array CGH is an important tool to refine minimal regions of deletions and to delineate genes, which potentially play a critical role in leukemogenesis. Both genes, in particular FBXL4, located in the smallest region of RMD at 6q in T-ALL defined so far, may be crucial for tumor development or progression and warrant further investigations to elucidate their possible implication in T-cell disease. 0010 IDENTIFICATION OF NOVEL RECURRENT GENOMIC ABERRATIONS BY ARRAY-CGH IN ADULT ACUTE LYMPHOBLASTIC LEUKEMIA A. Viardot, 1 C. Schwaenen, 1 N. Gökbuget, 2 D. Hoelzer, 2 M. Witzens-Harig, 3 H. Döhner, 1 S. Weßendorf, 1 M. Schmid1 1 2 Klinik für Innere Medizin III, ULM; Medizinische Klinik III, FRANKFURT; 3Medizinische Klinik und Poliklinik V, HEIDELBERG, Germany Background. In acute lymphoblastic leukaemia (ALL), genomic aberrations like translocations t(4;11) or t(9;22) are associated with an adverse prognostic impact and play an important role in the development of risk adapted treatment strategies. So far, chromosomal banding analysis is the standard cytogenetic procedure for routine diagnosis. Genomic array-comparative genomic hybridization (aCGH) has become a useful technique for genomic screening allowing a more precise delineation of small genomic aberrations. Methods. We analyzed 54 patients with ALL, which were treated within the GMALL trials, by aCGH analysis using a genomic 2,8K chip. Results. Forty-seven patients had a B-precursor- ALL including 14 patients with t(9;22) and 4 patients with t(4;11); 7 patients had a T-ALL. We found genomic aberrations in 37 out of 54 patients (69%). The most frequent aberrations were deletions on chromosome bands 9p21 (12 cases; 22%), 7q35 (9 cases; 17%) and 13q14 (8 cases; 15%); as well as gains on chromosome X, on chromosome arms 1q and 11q 13 (5 cases each, 9%). The consensus region of the 9p21 deletion was narrowed down to a size of 420 kilobasepairs. This region covers 3 different genes with potential tumor suppressor gene (TSG) function: p14ARF, p15INK4B/p10 and p16INK4A. Further consensus regions 4 | haematologica/the hematology journal | 2007; 92(s1) could be delineated which contains candidate gene of possible biologic importance: gains on chromosome bands 8q24 (C-MYC), 9q34 (ABL-1) and 11q13 (CyclinD1), deletions on chromosome bands 12p13.1 (CDKN1B) and 16q22 (TRADD). In the group of B-precursor-ALL, there was a tendency to a higher number of aberrations per case in the standard risk group (that means no t(9;22) and t(4;11)) in contrast to the t(9;22) positive group (2.2 vs. 1.2 aberrations per case). Deletions on 9p21 and 12p13 seems to be more frequent in the standard group than in the t(9;22) group (9p21: 10/27 vs. 1/14, p=0.06; 12p13: 5/27 vs. 0/14; p=0.14, Fisher´s exact test). Conclusions. aCGH analysis is useful for the identification of recurrent genomic aberrations which are not detectable using standard cytogenetic techniques. 0011 INV(11)(Q21Q23) FUSES MLL TO THE NOTCH CO-ACTIVATOR MASTERMIND-LIKE 2 IN SECONDARY T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA M. Metzler, 1 M. Staege, 2 L. Harder, 3 D. Mendelová, 4 J. Zuna, 5 C. Meyer, 6 T. Flohr, 3 J. Meerpohl, 7 D. Bednárová, 4 S. Gsek, 3 T. Langer, 1 J. Trka, 5 J Sterba, 4 J. Harbott, 8 R. Siebert, 3 R. Marschalek, 6 C.Niemeyer, 7 W. Rascher1 1 University of Erlangen, ERLANGEN, Germany; 2 Martin-Luther University Halle, HALLE, Germany; 3 University Hospital Schleswig-Holstein, KIEL, Germany; 4 University Hospital Brno, BRNO, Czech Republic; 5 Charles University, PRAQUE, Czech Republic; 6 University of Frankfurt, FRANKFURT, Germany; 7 University of Freiburg, FREIBURG, Germany; 8 University of Giessen, GIESSEN, Germany Development of a secondary leukemia after chemotherapeutic treatment for childhood acute leukemia is associated with rearrangements of the MLL gene on chromosome 11q23 and characteristically results in acute myeloid leukemia (AML). We identified the NOTCH co-activator Mastermind-like 2 as novel MLL fusion partner in two cases of pediatric therapy-related leukemia. The MLL-MAML2 fusion results from a cryptic inv (11)(q21q23). With a latency of twenty months after initial diagnosis of MLL negative AML and five years after precursor B acute lymphoblastic leukemia, respectively, both patients developed a therapyrelated T-cell acute lymphoblastic leukemia. MAML2 is the first MLL fusion partner involved in human NOTCH signaling and was only recently identified as recurrent translocation fusion partner in a subset of salivary gland tumors. The genomic MLL breakpoint shows similar localization and sequence features described for etoposide induced t- AML. The growth dynamic between primary and secondary disease was quantified using the individual genomic fusion sequence and Ig/TCR rearrangements as clonal markers. Whole genome expression profiles demonstrated involvement of target genes downstream of NOTCH, which suggests a modulatory role of the MAML2 transcriptional activation domain in MLL leukemogenesis and lineage assignment induced by the MLL-MAML2 fusion protein. 0012 CHARACTERISTICS OF MESENCHYMAL STROMAL CELLS FROM BONE MARROW OF CHILDREN WITH ACUTE LYMPHOBLASTIC LEUKEMIA H. Dimitriou, C. Perdikogianni, G. Martimianaki, D. Choumerianou, E. Stiakaki, S. Genitsari, M. Kalmanti University of Crete, HERAKLION, CRETE, Greece Background. The effect of several chemotherapeutic agents on mesenchymal stromal cells (MSC) has been tested in vitro and it was found that MSC are sensitive to different cytotoxic drugs. In the only existing in vivo study assessing MSCs properties from bone marrow (BM) of adult patients under chemotherapy though, such an effect was not observed. Aim. To detect a) any effects of the acute lymphoblastic leukemia on the morphology and functional characteristics of MSCs in children, b) alterations in MSC characteristics that could be attributed to chemotherapy and c) the possible bone marrow microenvironment restoration, if damaged, and the time point that this occurs. Material and Methods. BM mononuclear cells (MNC) from children with ALL [diagnosis (ALL_d, n=12), 15th day (d15, n=6), 33rd day of therapy (d33, n=9), maintenance (n=26) and end of therapy (ALL_end, n=11)] were cultured under conditions that favor MSC growth, for six passages (1-6). The cell doubling time (DT), the development of CFU-F colonies and surface antigen expression were evaluated in each treatment phase and in P2, P4 and P6. Moreover, apoptosis by 7AAD staining (flow cytometry) was assessed. Selected samples from each group were cultured under the appropriate conditions for adipocyte, osteocyte and chondrocyte differentiation.
Expression of the oncogene H-Ras and the tumor suppressor genes p53, p16 and Rb was assessed in both MSC_P2 and P6 and MNC of diagnosis. Results. MNC of diagnosis required more days to reach confluency (23.9±2.09) compared to MNCs from the groups corresponding to different stages of treatment, which required 16.9±0.6 days. DT, which at diagnosis had the highest value, (4.26±0.88 vs 2.34±0.32 d15, 2.95±0.45 d33, 3.52±0.54 remission, 2.94±0.31 ALL_end) increased with the progression of passages. The immunophenotypic analysis showed a homogenous cell population with MSC characteristics appearing as early as P1 (CD73, CD105, CD146>90%) and simultaneous absence of hemopoietic markers. The CD95 expression was found to be high (95.8±2.7% ALL_d, 95.6±3.6% ALL_end) whereas the rate of apoptosis was low (
Page 1 and 2: haematologica the hematology journa
Page 3 and 4: Information for readers, authors an
Page 5 and 6: EHA Executive Board E. Hellström-L
Page 7 and 8: Poster session I POSTER SESSION POS
Page 9 and 10: 12 th Congress of the European Hema
Page 11: dasatinib. Methods. We studied Ikar
Page 15 and 16: is the gene for the erythropoietin
Page 17 and 18: safety of a slow-release liposomal
Page 19 and 20: 0029 OUTCOME OF THE TREATMENT OF AD
Page 21 and 22: drug-induced apoptotic response of
Page 23 and 24: 41% in the PI3K- group (p=0.001). I
Page 25 and 26: Acute myeloid leukemia - Clinical I
Page 27 and 28: to 60 years (n=116, or 72%) receive
Page 29 and 30: 0056 PROGNOSTIC SIGNIFICANCE OF FLT
Page 31 and 32: Anemia and Bone marrow failure 0061
Page 33 and 34: tified with the current protocol. S
Page 35 and 36: new cases of lead poisoning due to
Page 37 and 38: icance, from baseline to week 6 (p
Page 39 and 40: 0086 THROMBELASTOGRAPHIC CHART RELI
Page 41 and 42: trials. The aim of this retrospecti
Page 43 and 44: tant function in this disease, nega
Page 45 and 46: ed to a favorable outcome. Bialleli
Page 47 and 48: stronger levels of p21 in the cell
Page 49 and 50: hematological centers in one countr
Page 51 and 52: ure 1). Conclusions. Results for re
Page 53 and 54: patients. After a median follow-up
Page 55 and 56: Cytogenetics and Molecular diagnost
Page 57 and 58: 0135 ROUTINE DETECTION OF CYTOGENET
Page 59 and 60: (MMolR, defined as a BCR-ABL x 100
Page 61 and 62: 0146 ARSENIC TRIOXIDE INDUCES ACCUM
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tinguish between genotypic B-cell l
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Genomics and proteomics 0158 PLASMA
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0164 EVALUATION OF MULTIPLEX LIGATI
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each patient’s replicate conditio
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0174 RELATION BETWEEN LOW PML-RARα
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0179 ESHAP VS GIN AS SALVAGE AND MO
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Immunology and gene therapy 0184 EA
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Cell viability was not affected by
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month is not relevant to chronic Gv
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Infection and supportive care I 020
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0206 POTENTIAL ROLE OF CMV IN THE O
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3H-thymidine uptake in cell culture
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0217 TUBERCULOSIS AMONG A COHORT OF
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0222 COMPARISON OF IWG 2006 AND IWG
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tem (IPSS) to h-MDS was also invest
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PCH97-19) were studied. Conventiona
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of erythroid colonies was reduced i
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0245 POTENT AND SELECTIVE INHIBITIO
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0250 INACTIVATION OF SUPPRESSOR OF
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Bortezomib 1.3 mg/m 2 days 1,4,8,11
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Response was defined according to E
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G-CSF can be used in neutropenic pa
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ence and functional activity of CD8
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itating tumor development, or engag
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phoma and SNT-13, -15 were establis
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usage (2/20 ie 10%) were observed.
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0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
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(range, 1-6) and 11 treatment cycle
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0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
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functional activity was confirmed b
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No major toxicity, neither hematolo
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enewal potential of X-RAR-positive
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(50-99) respectively. Serial analys
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cell-interaction, adhesion and acti
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0340 ALTERED FIBRIN CLOT STRUCTURE
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Conclusions. This study demonstrate
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0354 FACTOR V LEIDEN HOMOZYGOUS GEN
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Results. From July 2005 through Mar
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0364 CLINICAL EFFICACY OF OXALIPLAT
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one marrow and peripheral blood ste
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ecently suggested (Boissel et al.,
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0378 SAFETY AND EFFICACY OF THE TER
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Cytogenetics and molecular diagnost
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0385 CYTOPLASMIC MUTATED NUCLEOPHOS
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0390 ELTROMBOPAG RAISES PLATELET CO
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factor for the achievement of CR wa
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The cases of RAS showed two peaks o
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is 85%. Seven out of the 25 relapse
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0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
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successfully managed with GM-CSF di
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49% for PCR positive patients (95%
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+8 (1 PR+1 HI) and 14/24 pts with c
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(e.g. bcr-abl leading to CML). CSC
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0438 TERC MUTATIONS ANALYSIS IN PAT
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observed in all mice. Analysis of l
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ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
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One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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genesis of acute myeloid leukaemia
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polymorphism at nucleotide 4889 of
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expression along with a decreased C
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0487 MUTATIONAL STATUS OF NUCLEOPHO
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previously reported, a single cours
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0497 SINGLE AGENT CLORETAZINE (VNP4
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ly received melphalan-based chemoth
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were similar among the 3 groups. Ho
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Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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0523 DNA REPAIR INHIBITION IN RESTO
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held true when BMI-1 expression was
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Ph + cells in the bone marrow). We
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derivative chromosome (4p16, 7p14,
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0545 STABILIZED BONE MARROW IS NOT
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obtained in low (Sokal) risk patien
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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patients had died of their underlyi
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scripts and proteins most affected
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modulated after 24 h (37 up- and 59
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0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
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Results. A total of 396 patients we
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C30 questionnaire, and the correspo
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wave length of light of reflected r
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0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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BRIC 126 and 4N1K) in cells lacking
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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%
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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
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1230 ASSOCIATION OF HEPARANASE GENE
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posed, was: DF = (CD43%+FMC7%+CD79b
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treatment of acute promyelocityc le
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loaded group and 35 (70%) were non-
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mild. Fas and soluble Fas ligand le
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1265 POSACONAZOLE THERAPY IN REFRAC
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ly express the cytoplasmic (inactiv
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findings confirmed the significant
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a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
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1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
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phamide 750 mg/m 2 on day 1, vincri
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nomenon is unclear. It has been sug
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oped mild thrombocytopenia (platele
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gle dose of 54mg/m 2 rituximab furt
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patients (pts), 36 male, with acute
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esulting alterations of the endothe
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(range 1-7) and 28,6% of patients h
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three decades. In vivo, Ara-C is tr
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statistical analysis. Results. Seve
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Results. Though there was no recogn
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2% and 19% of patients with or with
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were older than 65 y) which can be
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1376 RESVERATROL INDUCED P53 MEDIAT
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median time of 21 days to reach >0.
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ly. Conclusions. 1. Combined intens
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to the presence of IVS1-6 mutation
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fy predictive factors for these abn
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acute leukemia. However, we cannot
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agents. They involve primarily the
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voriconazole for 2 months followed
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typed using a commercially availabl
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low up of ABL KD mutations’ level
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with development of BC/AP. 2. EVI-1
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1447 THE IMPACT OF DISPARITY IN SHO
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three had visual field defects, two
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acquired mutation most prone to cau
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1466 ROS GENERATION AND APOPTOSIS I
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1473 DIARRHEIC SYNDROME, A CLINICAL
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gene fusion is an independent progn
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1484 EPIDEMIOLOGY AND RESPONSE TO T
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1492 FREQUENCY OF MEDITERRANEAN GLU
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immune globulin was administered at
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maintained on Imatinib 400 mg. Afte
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Hodgkin’s disease is well known,
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gram provided a unique chance to de
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even when ADP-induced plt activatio
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medullary involvement of multiple m
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1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
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Bahr, J., 0148 Bai, M., 1551 Baia,
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Bottini, P.V., 1181 Botto, B., 0408
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Chaidos, A., 0456, 0498, 0599, 0686
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De Keersmaecker, K., 0442, 0875 De
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El-Sharkawy, N., 0016 Elwahidi, G.,
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Garcia-Frade, J., 0346, 0680, 1105
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Zouabi, H., 0503, 0999 Zoumbos, N.C
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12 th Congress of the European Hema
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12th Congress of the European Hematology ... - Haematologica

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