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12 th Congress of the European Hematology Association genetic mechanisms involved in the silencing of MHC2TA transcription in leukaemia T-cells also to histone modifications at the CIITA-PIII region. Using chromatin immunoprecipitation (ChIP) assays we found that the level of acetylated histone H3 in CIITA-PIII chromatin in T-leukaemia was strongly reduced when compared with CIITA-expressing T-lymphoma cells. The opposite was noted for the triple-methylated lysine 27 modification in histone H3. This modification is associated with compact chromatin and transcriptional silent genes. Subsequently, we also established by ChIP that the enhancer of zeste homolog 2 (EZH2), which has intrinsic histone methyltransferase activity, is recruited into CIITA-PIII chromatin in T-leukemia cells. Together our data reveal that, in addition to DNA methylation modifications, histone methylation modifications are associated with transcriptional silencing of MHC2TA in T-leukaemia and provide a link with components of the polycomb group family of proteins. 0930 UNCOVERING THE EPIGENETIC PATHOMECHANISM IN 13Q14 D. Mertens, 1 M. Ruppel, 2 A. Philippen, 3 C. Tschuch, 2 V. Fleig, 2 C. Mund, 2 F. Lyko, 2 B. Radlwimmer, 2 H. Döhner, 3 S. Stilgenbauer, 3 P. Lichter2 1 University Hospital Ulm, DKFZ Heidelberg, ULM; 2 DKFZ, HEIDELBERG; 3 University Hospital, ULM, Germany Introduction. Deletions in chromosomal band 13q14.3 distal to RB1 occur in a variety of human neoplasms like B-cell chronic lymphocytic leukaemia (CLL), indicating a tumor suppressor mechanism in this region. Intriguingly, several characteristics of the region of interest point to an epigenetic pathomechanism: i) candidate genes lack point mutations, yet ii) these genes are downregulated in tumors, iii) the presence of large noncoding RNA genes in 13q14.3 is reminiscent of imprinted regions where only one gene copy is active. The data we show here led us to propose a novel oncogenic mechanism where already in healthy tissue only one gene copy is active while one gene copy is randomly chosen for silencing. Loss of the single active copy is then sufficient for complete loss of gene function in tumor cells. Currently we are trying to identify the (epi- )genetic element that controls the whole locus. Aims. Identification of the epigenetic regulatory mechanism localized in 13q14.3. Methods and Results. We performed FISH analyses of hematopoietic and nonhematopoietic cell lines to assess replication timing and chromatin packaging of the critical region. In line with an imprinting mechanism, we find that the two copies of the critical region replicate asynchronously and/or show delayed chromatid segregation, suggesting differential chromatin packaging of the two copies of 13q14.3. Next, we found by sequencing of SNPs that 13q14.3 candidate genes are expressed from one copy only in healthy probands. However, expression originated from either the maternal or paternal copy, excluding an imprinting mechanism. In order to identify the regulatory element, we performed DNA methylation analyses and could show that one of the CpG islands of the region is methylated. We could also show a functional interconnection of DNA methylation and gene expression, as demethylating agents and histone hyperacetylation induced biallelic expression. However, replication timing was not affected. Currently we are employing array- and capillary electrophoresis-based analysis of DNA-methylation (aPRIMES and bio- COBRA) and chromatin-immunoprecipitation on arrayed CpG-libraries (chIP on chip) with antibodies specific for histone modifications in order to identify the epigenetic element regulating the critical region. Conclusions. We propose that differential replication timing represents an early epigenetic mark that distinguishes the two copies of 13q14.3, resulting in differential chromatin packaging and monoallelic expression. This has profound effects for the tumor suppressor mechanism localized in 13q14.3: Deletion of the single active copy of the region at 13q14.3, which is detected in more than 50% of CLL tumors, will suffice for complete loss of tumor suppressor function, as the remaining gene copies are epigentically silenced. In addition, we are currently identifying the locus control region that orchestrates gene expression in the critical region. Thus, we provide a model for the pathomechanism of 13q14.3 in CLL by the interaction of genetic lesions and epigenetic silencing. 0931 β-TRCP MEDIATES UBIQUITINATION AND DEGRADATION OF THE ERYTHROPOIETIN RECEPTOR AND CONTROLS CELL PROLIFERATION F. Verdier, L. Meyer, B. Deau, H. Forejtnikova, D. Dumenil, F. Margottin-Goguet, C. Lacombe, P. Mayeux Cochin Institute, PARIS, France Control of intensity and duration of erythropoietin (Epo) signalling 348 | haematologica/the hematology journal | 2007; 92(s1) is necessary to tightly regulate red blood cells production. After Epo stimulation of erythroid cells, 2 types of signal are transduced via the Epo receptor (Epo-R): positive signals involved in survival and proliferation, and negative signals involved in signal arrest. We have recently shown that the ubiquitin/ proteasome system plays a major role in the control of Epo-R signalling duration and desensitisation processes. Indeed, after Epo stimulation the Epo-R is ubiquitinated and its intracellular part is degraded by the proteasome, preventing further signal transduction. The remaining part of the receptor, together with associated Epo is internalised and degraded by the lysosomes (Walrafen et al. 2005 Blood, 105, 600-608). Our aim was to identify the E3 ubiquitin ligase involved in Epo-R ubiquitination. The Epo-R contains a putative β- Trcp binding site in its intracellular domain. Interestingly, this putative binding sequence is located in a region of the Epo-R that is deleted in erythroid progenitors from patients with familial polycythemia. We show that β-Trcp is responsible for Epo-R ubiquitination upon Epo stimulation. After Epo stimulation, β-Trcp binds to the Epo-R and this binding is dependent on Jak2 activation. Mutation of the Ser 462 residue of the Epo-R, located in the consensus β-Trcp binding site abolished β- Trcp binding, Epo-R ubiquitination and EpoR cleavage by the proteasome. Activation of the mutated Epo-R is prolonged in comparaison with Epo-R WT and BaF3 cells expressing this mutated receptor unable to bind β-Trcp are hypersensitive to Epo. Whether the removal of the β-Trcp binding site contributes to the hypersensitivity to Epo in familial polycythemia is currently under study. 0932 IDENTIFICATION OF PROTEIN TYROSINE KINASES THAT CAN SUPPORT THE PROLIFERATION AND SURVIVAL OF HEMATOPOIETIC CELLS E. Lierman K.U. Leuven, LEUVEN, Belgium Introduction. Protein tyrosine kinases are an important family of signaling proteins involved in the proliferation and survival of cells. They are frequently activated in leukemia through mutation or their involvement in chromosomal translocations often leading to fusion of kinase domains with homodimerization domains present in the partner genes. Examples of this are the BCR-ABL fusion in CML, the ETV6-PDGFRβ fusion in CMML, and the NPM-ALK fusion in ALCL. Aims/Methods. For many tyrosine kinases it remains unclear whether they can be activated by enforced homodimerization and whether these activated kinases would stimulate proliferation and survival pathways, leading to transformation of hematopoietic cells. To test this we generated fusions between the homodimerization domain of ETV6 and a variety of tyrosine kinase domains, and determined if expression of these constructs resulted in the transformation of Ba/F3 cells to IL3 independent growth. Results. As a first method, we performed a retroviral insertional mutagenesis screen for which we used a modified retroviral vector containing an exon encoding the homodimerization domain of ETV6 followed by an artificial splice donor site. When inserted in the host genome, this vector would drive the expression of a fusion transcript consisting of the exon encoding the homodimerization domain, and some exons of the gene in which the retrovirus was inserted. Using this screen, we obtained 423 independent Ba/F3 clones that were able to proliferate in the absence of IL3. 271 of these clones contained insertions in 8 different tyrosine kinase genes: Abl1, Fgfr1, Hck, Jak2, Lck, Mertk, Mst1r and Tnk1. In all these cases, the fusion between the homodimerization domain of ETV6 and the kinases were in-frame and the kinase domains were completely included in the generated fusion genes. In the other 152 Ba/F3 clones, no meaningful fusion transcripts could be detected. In a second method, we directly generated expression plasmids containing fusions between the homodimerization domain of ETV6 and different tyrosine kinase domains. So far, our results show that AXL, EPHA2, EPHB4, FGFR1, KIT, SRC, SYK, TYRO3, YES1 and ZAP70 all can be activated by homodimerization and support IL3-independent growth of Ba/F3 cells. When analyzing the activation of downstream signaling proteins such as PI3K, Akt, ERK, SRC kinases and STATs, significant differences were observed between these different oncogenic kinases. Conclusions. Our results identify a number of tyrosine kinase proteins that can be activated by homodimerization and lead to stimulation of proliferation and survival pathways in hematopoietic cells. Some of these tyrosine kinase genes are novel candidate oncogenes. The study of specific signaling pathways activated by these activated tyrosine kinases may be usefull for the design of novel therapies.
Publication Only 0933 CLINICAL FEATURES OF ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION- ASSOCIATED ORGANIZING PNEUMONIA K. Ohashi, 1 M. Jinta, 2 H. Akiyama, 1 H. Sakamaki1 1 Tokyo Metropolitan Komagome Hospital, TOKYO, Japan; 2 Tokyo Medical and Dental University, TOKYO, Japan In this study, we describe the clinical course and outcomes of allogeneic hematopoietic stem cell transplantation-associated organizing pneumonia (HOP) observed in our institution over the past 20 years. Charts and chest radiographs of 603 allogeneic transplant recipients were retrospectively reviewed for HOP. Total 12 cases of HOP were observed (2.0%) at a median interval of 148 days after transplantation (range, 53-475 days). They presented low-grade fever, non-productive cough and dyspnea at the onset of HOP. The initial antibiotics treatment did not ameliorate these symptoms, but most patients well responded to 0.5-1 mg/kg of prednisolone. However, in 9 out of 12 patients, HOP flared-up after discontinuing treatment or while decreasing the doses, but responded to the retreatment with the initial dose of steroids. Although 3 patients died, there was no death due to pulmonary failure. In remaining 9 patients, there was no relapse of primary disease and 5-year survival was 74.1%. The clinical features of 12 patients were similar in that they all received an irradiation containing conditioning and most patients had a prior history of acute graft-versus-host disease (GVHD) and cytomegalovirus (CMV) infection. Furthermore, 8 patients had active chronic GVHD at the onset of HOP. These suggest that several factor such as irradiation containing regimen, previous CMV infection and allogeneic immune reaction may contribute to the occurrence of HOP. Moreover, the patients with HOP might enjoy a relatively good prognosis due to low rate of relapse of primary disease possibly through graft-versus-leukemia reaction, even though facing multiple episodes of disease exacerbation of HOP. Table 1. Clinical features of HOP. 1 Day 105 + + - - 88 68 71/68 N M No No + - - 0.20 98.6 87.6 ND ND 2 Day 53 + + - - 96 33 33/531 A+I M No No + - - 0.38 130.3 78.0 68.2 73.2 3 Day 173 + + + - 91 14.3 35/541 A F No Yes + - + 0.06 133.9 72.1 85.7 88.7 4 Day 203 - - + - 96 2.3 ND/ND N M No No + - + ND 109.2 79.3 81.7 87.3 5 Day 140 + + - - ND 2.2 ND/ND A F No Yes - - + ND 109.2 77.6 ND ND 6 Day 259 - + - - 97 1.9 ND/ND N M No No - - + 0.14 103.9 88.4 94.2 93.7 7 Day 475 + - + - 81 35.1 6/134 A+I D No Yes + - + ND 122.0 83.5 ND ND 8 Day 124 + + - - 92 0.4 31/551 A+I D No Yes + - + 0.36 96.0 86.1 57.1 87.4 9 Day 156 - - + - 96 0.0 6/372 A+I M No No - + + 0.51 118.9 83.9 107.0 86.5 10 Day 118 - + + - 94 4.7 19/525 A+I M No Yes - + + ND 120.7 83.9 ND ND 11 Day 266 + + - - 92 1.1 90/765 I D No Yes - + - 0.10 104.9 81.3 51.0 76.0 12 Day 122 + + - - 91 14.4 ND/230 A+I M No Yes - + - ND 89.5 87.6 83.1 93.9 0934 B-CELL CHRONIC LYMPHOCYTIC LEUKEMIA-DERIVED DENDRITIC CELLS STIMULATE ALLOGENEIC T-CELL RESPONSE AND EXPRESS CHEMOKINES INVOLVED IN T-CELL MIGRATION W. Luczynski, A. Stasiak-Barmuta, J. Piszcz, E. Ilendo, O. Kowalczuk, M. Krawczuk-Rybak Medical University, BIALYSTOK, Poland Background. Despite discovery of new therapeutic agents, including nucleoside analogs and monoclonal antibodies, the B-cell chronic lymphocytic leukemia (B-CLL) remains incurable. In recent years, some effort has been made in developing T-cell specific immunity against neoplasmatic cells. Reconstitution of effective costimulation and immunological response of host T-cells against CLL cells could be a potential approach in immunotherapeutic trials. CD40/CD40L system is involved in the survival and proliferation of normal and neoplasmatic B-cells. Some preclinical studies have shown that CD40 stimulation can differentiate leukemic cells into dendritic cells (DCs) and result in host response. Aims. In this study, we sought to determine whether B-CLL cells could be turned into efficient and functional antigen presenting cells, as well as to assess the type of allogeneic T-cell response against B-CLL - derived DCs. Methods. B-CLL cells from 25 patients were stimulated or not with CD40L and IL- 4 for 96 hours and then cultured in mixed lymphocyte reaction (MLR) with allogeneic T-cells. The expression of costimulatory and adhesion molecules at mRNA (real-time RT PCR) and protein level (flow cytometry) was assessed before and after the culture of B-CLL cells with or without CD40L/IL-4. The expression of activation molecules on the surface of T-cells before and after MLR was assessed with flow cytometry. The mRNA levels for chosen chemokines was determined by real-time 12 th Congress of the European Hematology Association RT-PCR. Results. 1) after CD40 stimulation B-CLL cells achieved phenotypical and functional characterization of DCs (i.e. upregulated co-stimulatory and adhesion molecules at mRNA and protein level) 2) leukemiaderived DCs expressed higher amount of mRNA for chemokines involved in T-cell migration (MDC, TARC and CCR7) 3) the proliferating response of T-cells against leukemia-derived DCs consisted of CD4 and CD8 cells (upregulation of HLA-DR and OX40). Conclusion. Our experiment confirm that B-CLL cells can be turned into dendritic-like cells, additionally, these cells express chemokines involved in T-cell migration and stimulate allogeneic response. 0935 TRANSCRIPTIONAL SILENCING AND FREQUENT ABERRANT DNA METHYLATION OF ADAMTS-1, AN ANTIANGIOGENIC FACTOR WITH DIRECT INHIBITORY EFFECTS ON LEUKEMIC CELL GROWTH IN CHILDHOOD ACUTE LYMPHOBLASTIC LEUKEMIA K.-M. Lau, 1,3 L. Li1 , S.-H. Cheng1 , A.P.L. Cheung, 1 K.C.K. Cheng, 1 M.M.K. Shing, 2 C.-K. Li, 2 M.H.L. Ng1,3 1 Department of Anatomical and Cellular Pathology, 2 Department of Pediatrics, Prince of Wales Hospital, The Chinese University of Hong Kong and 3 State Key Laboratory in Oncology in South China, The Chinese University of Hong Kong Background. Angiogenesis plays an increasingly important role in carcinogenesis and is a prominent feature in the bone marrow (BM) in childhood acute lymphoblastic leukemia (ALL). ADAMTS-1 (A Disintegrin And Metalloproteinase with ThromboSpondin-like motifs-1) is a potent endogenous angiogenic inhibitor and its expression is down-regulated in certain human solid cancers. Aims. To examine the involvement of ADAMTS-1 in the pathogenesis of childhood ALL by expression and DNA methylation studies. Methods. Semi-quantitative RT-PCR was used for examining ADAMTS-1 expression. Bisulfite DNA sequencing and combined bisulfite restriction analysis for determining ADAMTS-1 methylation. Nucleofection, annexin V and propidium iodide staining for studying the effects of exogenic ADAMTS-1 expression on apoptosis and cell cycle regulation. Results. We first demonstrated aberrant DNA methylation associated loss of expression of ADAMTS-1 in 2/3 B-lineage ALL cell lines (Reh and RS4:11) and in 4/7 BM samples from pediatric patients with Blineage ALL, and reactivation of this gene expression by DNA demethylation in the Reh cells. We also first revealed aberrant DNA methylation of ADAMTS-1 in 31 out of 42 (74%) childhood patients with B-lineage ALL. Exogenic ADAMTS-1 expression significantly induced G2/M cell cycle arrest and apoptosis in the Reh leukemic cells. Conclusions. Our findings indicated that aberrant ADAMTS-1 DNA methylation associated transcriptional silencing of the gene might be involved in the leukemogenesis of childhood ALL. More importantly, in addition to the antiangiogenic effect, for the first time, we demonstrated the direct inhibitory effects of ADAMTS-1 on leukemic cell growth, which represents an endothelial cell-independent action of this molecule in cancer growth control. These findings may have critical impacts in molecular targeting strategy in the management of B-lineage childhood ALL. *The work described in this paper was partially supported by a grant from the Research Council of the Hong Kong Special Administrative Region, China (Project No. CUHK 4415/05M). haematologica/the hematology journal | 2007; 92(s1) | 349
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haematologica the hematology journa
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Information for readers, authors an
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EHA Executive Board E. Hellström-L
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Poster session I POSTER SESSION POS
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12 th Congress of the European Hema
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dasatinib. Methods. We studied Ikar
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Expression of the oncogene H-Ras an
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is the gene for the erythropoietin
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safety of a slow-release liposomal
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0029 OUTCOME OF THE TREATMENT OF AD
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drug-induced apoptotic response of
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41% in the PI3K- group (p=0.001). I
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Acute myeloid leukemia - Clinical I
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to 60 years (n=116, or 72%) receive
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0056 PROGNOSTIC SIGNIFICANCE OF FLT
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Anemia and Bone marrow failure 0061
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tified with the current protocol. S
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new cases of lead poisoning due to
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icance, from baseline to week 6 (p
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0086 THROMBELASTOGRAPHIC CHART RELI
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trials. The aim of this retrospecti
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tant function in this disease, nega
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ed to a favorable outcome. Bialleli
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stronger levels of p21 in the cell
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hematological centers in one countr
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ure 1). Conclusions. Results for re
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patients. After a median follow-up
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Cytogenetics and Molecular diagnost
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0135 ROUTINE DETECTION OF CYTOGENET
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(MMolR, defined as a BCR-ABL x 100
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0146 ARSENIC TRIOXIDE INDUCES ACCUM
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tinguish between genotypic B-cell l
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Genomics and proteomics 0158 PLASMA
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0164 EVALUATION OF MULTIPLEX LIGATI
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each patient’s replicate conditio
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0174 RELATION BETWEEN LOW PML-RARα
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0179 ESHAP VS GIN AS SALVAGE AND MO
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Immunology and gene therapy 0184 EA
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Cell viability was not affected by
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month is not relevant to chronic Gv
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Infection and supportive care I 020
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0206 POTENTIAL ROLE OF CMV IN THE O
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3H-thymidine uptake in cell culture
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0217 TUBERCULOSIS AMONG A COHORT OF
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0222 COMPARISON OF IWG 2006 AND IWG
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tem (IPSS) to h-MDS was also invest
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PCH97-19) were studied. Conventiona
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of erythroid colonies was reduced i
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0245 POTENT AND SELECTIVE INHIBITIO
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0250 INACTIVATION OF SUPPRESSOR OF
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Bortezomib 1.3 mg/m 2 days 1,4,8,11
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Response was defined according to E
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G-CSF can be used in neutropenic pa
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ence and functional activity of CD8
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itating tumor development, or engag
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phoma and SNT-13, -15 were establis
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usage (2/20 ie 10%) were observed.
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0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
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(range, 1-6) and 11 treatment cycle
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0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
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functional activity was confirmed b
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No major toxicity, neither hematolo
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enewal potential of X-RAR-positive
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(50-99) respectively. Serial analys
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cell-interaction, adhesion and acti
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0340 ALTERED FIBRIN CLOT STRUCTURE
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Conclusions. This study demonstrate
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0354 FACTOR V LEIDEN HOMOZYGOUS GEN
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Results. From July 2005 through Mar
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0364 CLINICAL EFFICACY OF OXALIPLAT
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one marrow and peripheral blood ste
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ecently suggested (Boissel et al.,
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0378 SAFETY AND EFFICACY OF THE TER
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Cytogenetics and molecular diagnost
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0385 CYTOPLASMIC MUTATED NUCLEOPHOS
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0390 ELTROMBOPAG RAISES PLATELET CO
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factor for the achievement of CR wa
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The cases of RAS showed two peaks o
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is 85%. Seven out of the 25 relapse
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0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
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successfully managed with GM-CSF di
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49% for PCR positive patients (95%
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+8 (1 PR+1 HI) and 14/24 pts with c
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(e.g. bcr-abl leading to CML). CSC
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0438 TERC MUTATIONS ANALYSIS IN PAT
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observed in all mice. Analysis of l
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ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
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One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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genesis of acute myeloid leukaemia
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polymorphism at nucleotide 4889 of
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expression along with a decreased C
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0487 MUTATIONAL STATUS OF NUCLEOPHO
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previously reported, a single cours
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0497 SINGLE AGENT CLORETAZINE (VNP4
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ly received melphalan-based chemoth
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were similar among the 3 groups. Ho
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Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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0523 DNA REPAIR INHIBITION IN RESTO
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held true when BMI-1 expression was
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Ph + cells in the bone marrow). We
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derivative chromosome (4p16, 7p14,
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0545 STABILIZED BONE MARROW IS NOT
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obtained in low (Sokal) risk patien
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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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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Page 309 and 310: p=0.014 and p=0.003, respectively).
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Page 401 and 402: 1063 ABNORMAL METHYLATION STATUS OF
Page 403 and 404: 1069 CLINICAL RELEVANCE OF REGULATO
Page 405 and 406: 1076 SERUM LEVELS OF SOLUBLE HLA CL
Page 407 and 408:
patient is still undergoing intensi
Page 409 and 410:
nificant MVD differences were detec
Page 411 and 412:
dictor of OS (p=0.004). High dose t
Page 413 and 414:
1099 ALTERATIONS IN THE NATURAL KIL
Page 415 and 416:
1105 CYTOGENETIC ABNORMALITIES IN 3
Page 417 and 418:
1110 CONSTITUTIVE ACTIVATION OF STA
Page 419 and 420:
efficacy results with a well-tolera
Page 421 and 422:
unmutated VH genes, and high and lo
Page 423 and 424:
Aims. Aim of this study was to pred
Page 425 and 426:
tested across a wide range of human
Page 427 and 428:
were incidentally diagnosed (52%).
Page 429 and 430:
ß2GP1 may be considered as determi
Page 431 and 432:
characterized in 198 β thalassaemi
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
Page 435 and 436:
to-pelvic or perineal trauma. No me
Page 437 and 438:
in age. High prevalence of LBM amon
Page 439 and 440:
ecause some of the patients were or
Page 441 and 442:
of the drug is crucial to allow lon
Page 443 and 444:
egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
Page 447 and 448:
admitted to ICU were discharged des
Page 449 and 450:
events -Postoperative states: 9,19%
Page 451 and 452:
efficacy and decreased atherosclero
Page 453 and 454:
1217 INCIDENCE OF EARLY STAGE IDIOP
Page 455 and 456:
1691GA and 1 homozygous 1691AA. The
Page 457 and 458:
1230 ASSOCIATION OF HEPARANASE GENE
Page 459 and 460:
posed, was: DF = (CD43%+FMC7%+CD79b
Page 461 and 462:
treatment of acute promyelocityc le
Page 463 and 464:
loaded group and 35 (70%) were non-
Page 465 and 466:
mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
Page 469 and 470:
ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
Page 475 and 476:
disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
Page 479 and 480:
phamide 750 mg/m 2 on day 1, vincri
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
Page 497 and 498:
Results. Though there was no recogn
Page 499 and 500:
2% and 19% of patients with or with
Page 501 and 502:
were older than 65 y) which can be
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
Page 505 and 506:
median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
Page 509 and 510:
to the presence of IVS1-6 mutation
Page 511 and 512:
fy predictive factors for these abn
Page 513 and 514:
acute leukemia. However, we cannot
Page 515 and 516:
agents. They involve primarily the
Page 517 and 518:
voriconazole for 2 months followed
Page 519 and 520:
typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
Page 523 and 524:
with development of BC/AP. 2. EVI-1
Page 525 and 526:
1447 THE IMPACT OF DISPARITY IN SHO
Page 527 and 528:
three had visual field defects, two
Page 529 and 530:
acquired mutation most prone to cau
Page 531 and 532:
1466 ROS GENERATION AND APOPTOSIS I
Page 533 and 534:
1473 DIARRHEIC SYNDROME, A CLINICAL
Page 535 and 536:
gene fusion is an independent progn
Page 537 and 538:
1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
Page 541 and 542:
immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
Page 545 and 546:
Hodgkin’s disease is well known,
Page 547 and 548:
gram provided a unique chance to de
Page 549 and 550:
even when ADP-induced plt activatio
Page 551 and 552:
medullary involvement of multiple m
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
Page 555 and 556:
1548 QUALITY ANALYSIS OF THE MULTID
Page 557 and 558:
Index of authors A Aapro, M., 0377,
Page 559 and 560:
Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
Page 567 and 568:
El-Sharkawy, N., 0016 Elwahidi, G.,
Page 569 and 570:
Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
Page 573 and 574:
Jaksic, B., 0127, 0446 Jaksic, O.,
Page 575 and 576:
Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
Page 581 and 582:
Musto, P., 0254, 0401, 0422, 0569,
Page 583 and 584:
Papadavid, E., 1442 Papageorgiou, E
Page 585 and 586:
Probatova, N., 0704 Prochazka, V.,
Page 587 and 588:
Rykavicin, O., 0504 Ryningen, A., 0
Page 589 and 590:
Sirard, C., 0127, 0128 Sirigou, A.,
Page 591 and 592:
Thiebaut, A., 0454 Thieblemont, C.,
Page 593 and 594:
Vincenzi, C., 1060 Viniou, N.-A., 0
Page 595 and 596:
Zouabi, H., 0503, 0999 Zoumbos, N.C
Page 597 and 598:
Page 599 and 600:
Page 601 and 602:
Page 603:
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