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12 th Congress of the European Hematology Association without PRF mutation showed normal PRF expression by flow cytometry; 2 patients showed A91V heterozygous polymorphism with reduced and absent PRF expression, respectively; 1 patient showed heterozygous G1070A mutation; genetic analysis could not be performed in 3 patients. Summary and Conclusions. In this series of patients the occurrence of HLH in adults was higher than expected and it was associated with a high incidence of lymphoma, also of B cell lineage, and of Herpes virus DNA detection. Impaired CTL appears to be, at least in some patients, independent from PRF mutations, raising the question of whether and how these genetic events can be related, in acquired HLH of adults, to the deficiency of the lytic activity of PRF. 0286 THE PROGNOSTIC SIGNIFICANCE OF CELL CYCLE REGULATORY GENES EXPRESSION IN DIFFUSE LARGE B-CELL LYMPHOMAS F. Kontsioti, 1 P.V. Pappa, 1 R.D. Rontogianni, 2 P.S. Papageorgiou, 1 E.C. Economopoulou, 1 T.P. Tsirigotis, 1 K.E. Kavada, 1 G.V. Giannopoulou, 1 K.I. Kaitsa, 1 G.K. Girkas, 1 P.E. Papageorgiou, 1 D.J. Dervenoulas,1 E.T. Economopoulos1 1 2 Attikon University General Hospital, ATHENS; Evangelismos Hospital, ATHENS, Greece Background. Diffuse large B-cell lymphoma (DLBCL) is an aggressive malignancy of mature B cells with heterogeneous prognosis. Biological markers have been used in an attempt to improve the discriminative capacity of the International Prognostic Index (IPI). Abnormalities of cell cycle constitute a marker of clonal expansion and may contribute to disease progression; thus the investigation of cell cycle regulatory genes may be of prognostic relevance. Aims. The aim of the present study was the investigation of gene expression levels of cell cycle regulatory genes in DLBCL and their relation to prognosis. Methods. The analysis included 45 newly diagnosed cases of diffuse large B-cell lymphomas and 15 cases of non-neoplastic lymphadenopathies used as controls. The IPI was available for all lymphoma cases. RNA was extracted from fresh frozen tissues and analyzed by RNase Protection Assay (RPA) with Riboquant kit (BD Biosciences). Two sets of probes were used that included cyclins, cyclin dependent kinases and their inhibitors. In more detail h-CC1 set of probes detected mRNA for the genes cdk-1,cdk-2,cdk-3,cdk- 4,p16,p27,p21,PISSLRE and h-CYC1 set of probes detected mRNA for the genes of cyclins A,B,C,D1,D2,D3 and A1.The intensity of each band was compared to that of the housekeeping genes GAPDH and L32 using the Image Master Software(Pharmacia). Moreover, immunohistochemistry was performed on paraffin-embedded tissue sections in order to verify the expression of germinal center proteins, bcl6 and CD10. Results. The expression levels of the cell cycle regulatory genes did not correlate with any of the clinical parameters nor the prognostic markers. 85% of patients that didn’t have complete remission to first line therapy, expressed the cyclinA1 (p=0,03). 92% of the patients with low IPI (0,1) expressed PISSLRE, while only 56% of the patients with high IPI (2,3,4,5),expressed this gene. Moreover, cdk2 and cdk4 expression levels were significantly higher in cases expressing bcl-6 protein (p=0,013, p=0,004 respectively). The mean expression level of cyclin B was higher in cases with positive expression of protein CD10 (p=0,007). All patients with negative expression of CD10 had a lower expression level of cyclinA1 compared to normal RNA pool (p=0,037). Moreover, patients expressing cyclinA1 had significantly shorter disease free survival (p=0,03), while the expression of PISSLRE was associated with significantly better overall survival (p=0,0329). Summary and Conclusions. Taking into consideration the heterogeneity of clinical behaviour of DLBCL, the cell cycle regulatory genes may serve as biologic markers with prognostic significance. Our study has shown that the expression level of cyclinA1 is associated with significantly lower response to first line therapy and lower disease free survival. Moreover the expression of PISSLRE seems to be associated with low risk disease and higher overall survival, which emphasizes the potential role of this gene as a tumour suppressor. 0287 Z-GUGGULSTERONE DOWNREGULATES SURVIVIN AND INDUCES CELL DEATH IN LARGE B CELL LYMPHOMA CELLS IN VITRO M. Angelopoulou, K. Lilakos, V. Salpeas, S. Sachanas, T.P. Vassilakopoulos, M.P. Siakantaris, M.N. Dimopoulou, P. Korkolopoulou, P. Panayiotidis, G.A. Pangalis University of Athens, ATHENS, Greece Background. Survivin is a member of the Inhibitor of Apoptosis Pro- 104 | haematologica/the hematology journal | 2007; 92(s1) teins and has recently gained attention as a possible therapeutic target in neoplasia, due to its dual role both as an antiapoptotic protein and as a cell cycle regulator. It is overexpressed in malignant cells and confers resistance to chemotherapy and other stimuli triggering apoptosis. Survivin as well as other antiapoptotic proteins are under NF-κB control. Z- Guggulsterone (Z-GGS) is a plant sterol, which has been used in inflammatory conditions, is a potent NF-κB suppressor and might affect Survivin. Aims. To evaluate Survivin expression by two large B cell lymphoma cell lines and study the effect of Z-GGS on Srvivin expression and cell viability. Methods. DB and HT cell lines were treated with increasing concentrations (10 µM, 20 µM and 30 µM) of Z-GGS, for 24, 48 and 72 hours. Survivin expression was tested by flow Cytometry and quantitative real time PCR using the Universal Probe Library hydrolysis probes and expressed as Survivin/abl ratio. Cell viability was assessed by the MTT assay. Results. Both cell lines were positive for Survivin at baseline by flow cytometry (66% of total cells for DB and 95% for HT). Treatment of DB cells with 10, 20 and 30Ìª Z-GGS resulted in a 44%, 49% and 68% reduction of Survivin expression at 24 hours, respectively, whereas the effect on HT was less prominent with a 10% reduction at 24 hours with 30 µM Z-GGS. Survivin transcripts decreased as well, with the maximum effect observed at 72 hours with 3 µM Z-GGS for both cell lines: Survivin/abl was 0.009 for untreated cells vs 0.0008 with 30 µM Z-GGS for DB cells and 0.0135 vs 0.0005 for HT cells. Linearity was observed for increasing concentrations of Z-GGS at 72 hours. Cell viability was practically unaffected at any time point with 10 and 20 µM Z-GGS for both cell lines, whereas 30 µM Z-GGS resulted in a 63% and 78% cell death at 48 and 72 hours respectively for DB cells and 67% and 83% for HT cells. Conclusions. The steroid Z-GGS downregulates Survivin expression in B-lymphoma cells in vitro and induces cell death at 30 µM concentration. Further experiments will clarify its possible role in the treatment of B-cell malignanciies 0288 CD5 POSITIVE SPLENIC MARGINAL ZONE LYMPHOMA : CLINICAL, CYTOLOGICAL, IMMUNOLOGICAL, MOLECULAR AND CYTOGENETICAL FEATURES OF A SERIES OF 35 CASES M. Baseggio, F. Petinataud, E. Callet-Bauchu, F. Berger, A. Traverse-Glehen, C. Thieblemont, D. Morel, G. Salles, P. Felman Centre Hospitalier Lyon-Sud, PIERR-BENITE, France Splenic marginal zone B-cell lymphoma (SMZL) has been recently recognized owing to clinical, cyto-histological, immunological, cytogenetical characteristics. The immunological profile, usually CD5, CD10, CD23, CD43, cyclinD1 negative B-cells, is however in lack of specific markers which could be useful in doubtful cases. For instance, the report of CD5 positive cases without histological control is still a matter of debate, and in fact the differential diagnosis with B-CLL or MCL is sometimes difficult. Nevertheless CD5 postivity has been reported in some histologically typical MZL cases and proposed as a marker for a more aggressive and disseminated disease. Here we described a series of 35 CD5 positive SMZL histologically proven in 26 cases and without t(11;14) detected by FISH, that were compared to a series of 44 typical CD5 negative SMZL. From a clinical, cytological and immunological point of view, the CD5 positive SMZL cases presented many similarities with the group of CD5 negative SMZL. The main differences consisted in a higher lymphocytosis at diagnosis (4,95 G/L in CD5 positive group and 1,60G/L in CD5 negative group, respectively -p=0.003-) and a more frequent IgM isotype of the monoclonal component (75% vs 53%). Interestingly, all CD5 positive cases in peripheral blood were CD5 positive on splenic specimen studied by flow cytometry and no CD5 negative B-cells were detected in spleen compartment. The tumoral mass assessed by spleen weight seemed similar between both groups.These results suggest that CD5 expression gives B-cells a higher propensity to recirculate from spleen. A good correlation was observed with the CD5 expression detected by immunohistochemistry. The few CD5 negative cases on sections corresponded in fact with a faint CD5 expression by FCM. Karyotypic changes were similar in both groups and included the chromosomal abnormalities previously described in SMZL. However, some differences were observed : trisomy 18 was more frequent (29% vs 11%) and the 7q deletion was less frequent (23% vs 36%) in the CD5 positive group than in the CD5 negative group, respectively. The frequency of 17p deletion, leading to an alteration of P53 and a more aggressive clinical course was similar in both groups. Most cases were mutated in the CD5 positive group (82%) in contrast to the CD5 negative group (55%). The IgVH analysis showed a VH4 usage gene in 4 cases (23%) of the 17 available CD5 positive cases, whereas in the CD5 negative group, an underrepresentation of VH4
usage (2/20 ie 10%) were observed. No difference in outcome and overall survival was found between both groups. In conclusion, this study allowed to confirm the existence of CD5 positive SMZL, closely related to classical CD5 negative SMZL and distinct from CLL and MCL. The differences observed with CD5 negative cases, in particular cytogenetical abnormalities and usage of IgVH gene, suggest that this entity may arise from a distinct cell in the marginal compartment, Obviously further studies of more cases are required to confirm and precise these data. 0289 ABERRANT METHYLATION OF SHP-1 (SH2-CONTAINING PHOSPHATASE 1) AND SOCS-1 (SUPPRESSOR OF CYTOKINE SIGNALLING 1) GENES IN IMMUNODEFICIENCY-RELATED LYMPHOMAS M. Cerri, 1 C. Deambrogi, 1 D. Rossi, 1 M. Lunghi, 1 P. Zigrossi, 1 V. Spina, 1 L. De Paoli, 1 P. Riccomagno, 1 A. Gloghini, 2 M. Lucioni, 3 D. Capello, 1 M. Paulli, 3 A. Carbone, 4 G. Gaidano1 1 University of Eastern Piedmont, NOVARA; 2 Division of Pathology CRO, AVIANO; 3 Division of Pathology IRCSS San Matteo, PAVIA; 4 Division of Patholohy, Nat.Cancer Inst., MILAN, Italy Background. SHP-1 and SOCS-1 are members of a family of negative regulators of signalling that act downstream of cytokine receptors, receptor tyrosine kinases and receptor complexes of the immune and hematopoietic system. SHP-1 and SOCS-1 act through the inhibition of the JAK2/STAT pathway and their inactivation is considered to be a relevant mechanism in JAK2/STAT pathway induction. Several observations point to induction of the JAK/STAT pathway as an important mechanism of lymphomagenesis. Aims. Since DNA methylation and DNA somatic mutation are mechanisms of gene silencing and gene inactivation involved in the pathogenesis of human cancers, including lymphoma, here we tested the involvement of SHP-1 and SOCS-1 methylation and of SOCS-1 mutation in immunodeficiency-related lymphoma. Methods. Tumor samples from 48 HIV-related non-Hodgkin lymphoma (HIV-NHL) and 25 post-transplant lymphoproliferative disorders (PTLD) were analyzed for SHP-1 and SOCS-1 methylation by methylation-specific polymerase chain reaction and for SOCS-1 mutation status by DNA direct sequencing. The tumor panel included 21 HIV-diffuse large B cell lymphoma (HIV-DLBCL), 17 HIV-Burkitt lymphoma (HIV-BL), 10 HIVprimary effusion lymphoma (HIV-PEL), 10 PTLD-immunoblastic (PTLD- IB), 7 PTLD-centroblastic (PTLD-CB), 4 polymorphic PTLD (P-PTLD), 3 PTLD-BL, and 1 PTLD multiple myeloma (MM). Results. Among HIV- NHL, SHP-1 methylation occurred in 23/48 (48%) cases, including 12/21 (57%) HIV-DLBCL, 3/17 (17.6%) HIV-BL, and 8/10 (80%) HIV-PEL. SOCS-1 methylation occurred in 7/48 (14.6%) HIV-NHL, including 5/10 (50%) HIV-PEL and 2/21 (9.5%) HIV-DLBCL. When considering EBV status, SHP-1 was methylated in 10/11 (91%) EBV-negative HIV-NHL and in 12/22 (54%) EBV-positive HIV-NHL. Among PTLD, SHP-1 methylation was detected in 19/25 (76%) cases, including 7/10 (70%) PTLD- IB, 6/7 (86%) PTLD-CB, 3/4 (75%) P-PTLD, 2/3 (66%) PTLD-BL and 1 PTLD MM. SOCS-1 methylation was detected in 3/25 (12%) PTLD, including 2/10 (20%) PTLD-IB and 1/7 (14.3%) PTLD-CB. When considering EBV status, SHP-1 was methylated in 12/13 (92%) EBV-negative PTLD and in 6/11 (54%) EBV-positive PTLD. Missense mutations of SOCS-1 were detected in 1/15 HIV-DLBCL tested and in 1/25 PTLD. Conclusions. The implications of our data are threefold. First, SHP-1 methylation is involved in the majority of HIV-NHL and PTLD. Second, it is remarkable that virtually all EBV-negative HIV-NHL and EBV-negative PTLD carry SHP-1 methylation. In EBV-positive B-cells, EBV infection activates the STAT pathway. It is conceivable that, in EBV-negative HIV-NHL and in EBV-negative PTLD, SHP-1 inactivation through aberrant methylation may surrogate EBV infection for STAT activation. Third, similar to observations in NHL of the immunocompetent host, SOCS-1 methylation and mutation is rarely implicated in the pathogenesis of immunodeficiency-related NHL. This notion is consistent with the phenotype of SOCS1-deficient mice, that die of a myeloproliferative disease but do not develop a lymphoproliferative disease 0290 P53 STABILIZATION BY THE MDM2 INHIBITOR NUTLIN-3A INDUCES P53-DEPENDENT CELL CYCLE ARREST AND APOPTOSIS IN ANAPLASTIC LARGE CELL LYMPHOMA G. Rassidakis, V. Atsaves, E. Drakos, G. Georgakis, L.J. Medeiros, M.D. Anderson Cancer Center, HOUSTON, USA Background. Mutations of the p53 tumor suppressor gene is the most frequent genetic alteration in human cancer. However, p53 mutation rate is relatively low in most haematologic malignancies including non- 12 th Congress of the European Hematology Association Hodgkin lymphomas. Previously we have shown that p53 mutations are uncommon in anaplastic large cell lymphoma (ALCL), an aggressive T/null cell lymphoma type, despite the variable level of expression of wild-type p53 protein [Leukemia 2005;19(9):1663]. MDM2 (HDM2 in humans) is a physiologic negative regulator of p53 levels within the cell. We hypothesized that p53 stabilization using a novel Mdm2 inhibitor, nutlin-3A, would activate p53-dependent apoptotic and cell cycle regulatory pathways in ALCL cells carrying wild-type and potentially functional p53 gene. Methods. Two ALCL cell lines, SupM2 and DEL, carrying wild-type p53 (wt-p53) and 2 ALCL cell lines harboring a mutated p53 (mt-p53) gene, Karpas 299, and SR-786, were used. All cell lines were treated with different concentrations of nutlin-3A (0, 2.5 , 5, 10 mM). The effects of p53 stabilization by nutlin-3A on cell viability and proliferation of ALCL cells were assessed using trypan blue and MTS assays, respectively, at two time points (24 and 48 hours). Cell cycle and apoptosis (annexin V binding) analysis was also performed using flow cytometry. To further investigate the underlying mechanisms of cell cycle arrest and apoptosis following nutlin-3A treatment, Western blot analysis was performed. Results. Treatment with increasing concentrations of nutlin-3A resulted in a dose-dependent increase of p53 levels, which was associated with increased levels of MDM2 a known transcriptional target of p53 gene. P53 stabilization resulted in a concentration-dependent decrease in cell viability and total cell number in ALCL cells carrying wt-p53 (SupM2 and DEL) but not in cells harboring p53 mutations (Karpas 299 and SR-786). At a concentration of 10 mM nutlin-3A, cell viability was dramatically decreased at 48 after treatment in SupM2 and DEL. Changes in cell viability were largely attributed to apoptosis, since the percentage of Annexin V+ cells was increased from 8% to 87% in SUPM2 and from16% to 50% in DEL.. By contrast, no changes in cell viability or apoptosis were observed in Karpas 299 and SR-786 cell lines(mt-p53). Apoptosis was associated with cleavage of caspase 3 and 9 in immunoblots. Cell cycle analysis revealed that nutlin-3A treatment in SupM2 and DEL resulted in cell cycle arrest. The Sphase fraction of cell cycle was decreased by approximately 50% at a concentration of 5 mM, 24 hours following treatment. Cell cycle arrest was associated with a concentration-dependent increase of the cyclindependent kinase inhibitor p21, which is trancriptionally regulated by p53 gene. Conclusions. Selective inhibition of Mdm2 by nutlin-3A leads to non-genotoxic activation of p53 pathway and may represent a novel therapeutic modality in patients with ALCL. 0291 PREVALENCE OF CHLAMYDIA PSITTACI INFECTION IN NODAL AND EXTRANODAL NON-HODGKIN LYMPHOMAS J.M. Ferreri, 1 R. Dolcetti, 2 M. Guidoboni, 2 M.G. Cangi, 1 L. Pecciarini, 1 G.P. Dognini, 1 P.P. Ghia, 1 M. Malnati, 1 E. Pasini, 2 C. Doglioni, 1 M. Ponzoni1 1 2 San Raffaele Scientific Institute, MILAN; Centro di Riferimento Oncologico, AVIANO, Italy Background. Ocular adnexal lymphomas (OAL) are malignancies with rapidly increasing incidence rates. Recently, we demonstrated an association between Chlamydia psittaci (Cp) persistent infection and OAL. The condition of the systemic subclinical Cp infection encountered in many OAL patients provided the rationale for searching alternative sites of lymphoma development, an uncovered issue particularly for extranodal localizations. Methods. 172 non-consecutive cases of non-Hodgkin lymphomas were analyzed. Thirty-one patients with non-specific tonsillitis, 36 with non-specific reactive lymphadenopathies and 7 non-neoplastic spleens were used as controls (n=74). After central pathology review, DNA was extracted from formalin-fixed, paraffin-embedded tissue blocks and amplified by a multiplex touchdown PCR assay, which simultaneously detects the DNA of the three major Chlamydiae species (i.e. C. trachomatis, pneumoniae, and psittaci). DNA of C. trachomatis L2, C. pneumoniae TW-183 or C. psittaci ORNI were included as positive controls. Amplicons encompass part of the 16S rRNA gene and the 16S-23S spacer region in the ribosomal genes. PCR products were analyzed by electrophoresis and DNA fragment size was quantified by image analysis. Samples were considered positive when Chlamydia DNA was amplified in at least two of three independent experiments. Specificity of the amplified fragments was confirmed by direct sequencing. Sequence specificity was assessed by BLAST search. In each sample negative to PCR, amplification of α-globin control gene was carried out. Prevalence of Cp DNA for each lymphoma category was compared with the prevalence in the 74 controls. Results. Overall, Chlamydiae DNA was detected in 20 (12%) cases of NHL. Cp turned out to be the most haematologica/the hematology journal | 2007; 92(s1) | 105
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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
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 and 98: 0245 POTENT AND SELECTIVE INHIBITIO
Page 99 and 100: 0250 INACTIVATION OF SUPPRESSOR OF
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: phoma and SNT-13, -15 were establis
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
Page 149 and 150: 0385 CYTOPLASMIC MUTATED NUCLEOPHOS
Page 151 and 152: 0390 ELTROMBOPAG RAISES PLATELET CO
Page 153 and 154: factor for the achievement of CR wa
Page 155 and 156: The cases of RAS showed two peaks o
Page 157 and 158: is 85%. Seven out of the 25 relapse
Page 159 and 160: 0409 FRACTIONATED RADIOIMMUNOTHERAP
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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
Page 347 and 348:
2004 to January, 2006. At enrollmen
Page 349 and 350:
with a p value of ≥ 0.10. Sets of
Page 351 and 352:
BRIC 126 and 4N1K) in cells lacking
Page 353 and 354:
sclerosis[NS] and 12 Mixed cellular
Page 355 and 356:
0927 MK-0457, A NOVEL MULTIKINASE I
Page 357 and 358:
Publication Only 0933 CLINICAL FEAT
Page 359 and 360:
HSCT from the available Asian as we
Page 361 and 362:
that the incidence of JAK2 mutation
Page 363 and 364:
without type 2 diabetes. Methods. T
Page 365 and 366:
pts (38.8%) that were isolated (abs
Page 367 and 368:
y using the Miltenyi CD34 isolation
Page 369 and 370:
0969 COMPARISON OF CD25 IMMUNOHISTO
Page 371 and 372:
cytes was 24 days (range 8-32 days)
Page 373 and 374:
a cytogenetic hallmark for M4/M5 su
Page 375 and 376:
normal human BM B progenitor cells
Page 377 and 378:
0994 INCIDENCE OF INVASIVE ASPERGIL
Page 379 and 380:
3 of disease relapse.TRM at day+100
Page 381 and 382:
survival of five years. This dismal
Page 383 and 384:
1011 FLOW CYTOMETRIC DNA INDEX AND
Page 385 and 386:
1018 THE EFFECT OF THE SUGARBAKER P
Page 387 and 388:
1024 KIR/HLA CLASS I MISMATCHING AN
Page 389 and 390:
ment details and thrombotic histori
Page 391 and 392:
1036 INCIDENCE AND SPECTRUM OF INFE
Page 393 and 394:
tinely by our stem cell lab prior t
Page 395 and 396:
tion to a translocation t(5;14)(q35
Page 397 and 398:
ment of CML and induces a high rate
Page 399 and 400:
due to reactivation and/or progress
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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