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12 th Congress of the European Hematology Association sions. We conclude that syndecan-1, like the better recognised β2-M, CRP and IL-6 markers, has a prognostic value for the evolution of monoclonal gammopathies. 0280 HIGHLY PRESERVED POLYCLONAL REGULATORY T CELLS (TREGS) CAN DOMINATE EFFECTOR FUNCTIONS IN MULTIPLE MYELOMA PATIENTS M. Foglietta Division of Hematology, TORINO, Italy Naturally occurring CD4 + CD25 + T regulatory cells (Tregs) are a subpopulation of CD4 + T cells vital to homeostasis and maintenance of tolerance. Tregs play a key role in hampering anti-tumor immune surveillance by regulating T-cell immune responses against tumor cells. Depletion of Tregs brings to improved anti-tumor immune responses in both preclinical and clinical settings. Contradictory data have been reported in the frequency and function of Tregs cells in multiple myeloma (MM). The aim of this study was to characterize MM Tregs from the phenotypic, molecular and functional standpoints. We studied both peripheral blood (PB) and bone marrow (BM) samples from patients with symptomatic MM and from healthy donors. CD4 + CD25high Tregs were normally represented in both PB and BM of MM patients and expressed a memory and activated phenotype. No differences were observed between PB and BM Tregs of healthy donors and MM patients, based on the expression of CD45R0, HLADR, CD40L and CD69 cell surface antigens. Flow cytometry was also used to assess the intracellular expression of Foxp3, a transcription factor which has been shown to be crucial for the inhibitory function of Tregs cells. More than 90% of CD4 + CD25high T cells were Foxp3-positive in PB and BM of MM patients and healthy donors. Numbers and distribution of BM Treg were further confirmed by immunohistochemical analyses of Foxp3-positive cells in whole tissue paraffine embedded sections. CD4 + CD25 + T cells were purified from PB of newly diagnosed MM by MACS sorting. These cells were anergic to the stimulation via TCR and they were as effective as normal donor-derived CD4 + CD25 + cells in inhibiting the TCR-mediated proliferation of autologous CD4 + CD25 – counterparts. Moreover MM Tregs equally inhibited autologous and allogeneic CD4+CD25from normal donors. To investigate whether clonal restriction had occurred in MM Tregs, we studied TCR diversity of CD4 + CD25 + and CD4 + CD25 – cells by determining the reciprocal usage of BV gene segments (TCRBV repertoire) with a novel multiplex polymerase chain reaction assay, Our results demonstrate an highly preserved polyclonal TCRBV repertoire, providing the first evidence in cancer patients that TCR diversity of Tregs is not skewed by the long lasting exposure to tumor cells. Based on these data, we propose that inhibitory signals delivered by the highly preserved Tregs subset in MM can easily overwhelm the effector mechanisms of antitumor immunosurveillance which are deeply compromised in MM. Thus, depletion or neutralization of Tregs should be considered in future trials aimed at controlling the disease in MM patients by immune intervention. 102 | haematologica/the hematology journal | 2007; 92(s1) Non-Hodgkin lymphoma - Biology 0281 PERSISTENCE OF LYMPH NODE T(14;18) BEARING CELLS IN FOLLICULAR LYMPHOMA PATIENTS IN CLINICAL COMPLETE REMISSION: PROOF OF PRINCIPLE FOR MAINTENANCE THERAPY? J. Mayer, A. Janikova, L. Kren, D. Dvorakova, I. Kroupova, J. Smardova, J. Neubauer, I. Vasova University Hospital Brno, BRNO, Czech Republic Background. Despite many new therapeutic options, follicular lymphoma (FL) is a chronic relapsing malignant disease rarely cured by conventional treatments. Some institutions use PCR t(14;18) blood and/or bone marrow monitoring, however, its real importance remains controversial. Aims. We hypothesized that lymph nodes are much more better compartment for FL monitoring than peripheral blood/bone marrow. We asked whether it would be possible to monitor regularly the disease in patients by ultrasound-guided fine needle aspirations (UG- FNA) like we usually monitor acute leukemias by bone marrow aspirations. Methods. First we asked about the efficacy of FNA to detect FL by FISH and/or PCR. For this purpose we investigated either autopsy material or surgically removed lymph nodes both by FNA and classical histology.Then, upon informed consent, we performed UG-FNA in patients either with advanced disease or in clinical remission in order to search for lymph node t(14;18) bearing cells in involved nodes, or in previously involved node areas. Real time (RQ) PCR (Taqman) gives results as copies/106 cellular equivalents. Results. In 22 tested paired samples (histology vs. FNA) by PCR, 20/22 samples gave identical results. In one case each, histology vs. FNA or vice versa, gave discordant negative results. We performed 31 UG-FNA on out-patients basis without any complications. In 15 cases, both FISH and PCR were available, with FISH being positive in 13/15 samples and PCR in 8/15 samples. In only 4/31 cases, the FNA was not eventually carried-out for very small nodes. In 3/31 samples, the material did not contain vital nodal cells. All unsuccessful UG-FNA were performed in patients in remission (see below). Therefore, 24/31 samples could be examined by FISH and/or PCR: 10/24 in newly diagnosed patients, 9/24 in relapsed patients, and 5/24 in patients in remission. RQ PCR gave much higher copy numbers in lymph nodes (median: 2.3×106 )> bone marrow (16×103 )>peripheral blood (4.2×103 ). There were 12 UG-FNA in 11 remission patients (CT and usually also PET, and PCR from blood/or marrow, when available). 4/12 were technically unsuccessful and 3/12 samples did not contain material suitable for further examination. Four of these 7 patients had had PCR positivity at the time of diagnosis, and 6/7 are still in sustained remission. In 5 aspirations in 4 patients, there was detection of t(14;18). One patient is in long lasting remission despite two UG-FNA positive Results. Remarkably all other 3 patients relapsed 3, 6, and 12 months after an UG-FNA. Summary. This study is the proof of principle of the detection of residual (lymphoma progenitor, stem?) t(14;18) bearing cells in the previously involved lymph nodes despite patients being in well defined remission. Further study is needed to define the biological and clinical importance of this finding. This study is also the theoretical basis for maintenance therapy with rituximab, however, with the current strategy, some patients might be overtreated and the best schedule is not known. Supported by Research Grant MSM 0021622430. 0282 NK-CELL ASSOCIATED RECEPTORS EXPRESSION IN EPSTEIN-BARR VIRUS-POSITIVE GAMMA-DELTA T-CELL LINES DERIVED FROM PATIENTS WITH NASAL T-CELL LYMPHOMA AND CHRONIC ACTIVE EBV INFECTION Y. Zhang Tokyo Medical University, TOKYO, Japan Background and Aim. The contribution of chronic antigen stimulation to the occurrence of lymphoproliferative disorder (LPD) with the γ-δ Tcell lineage is unclear, despite the fact that Epstein-Barr virus (EBV) positive T-cell LPD is derived from antigen-stimulated cytotoxic T-cells. Given the possible association of antigen stimulation with the development of cytotoxic T-cell LPD, we compared gene expression patterns in Epstein-Barr virus (EBV)-positive γ-δ T-cell lines derived from patients with nasal T-cell lymphoma and chronic active EBV infection and those in γ-δ T-cells from healthy volunteers. [METHODS] Three EBV-positive γ-δ T-cells lines, SNT cells (SNT-8, SNT-13 and SNT-15), were used in this study. SNT-8 was established from patients with nasal T-cell lym-
phoma and SNT-13, -15 were established from patients with chronic active EBV infection (Zhang Y, et al., Br J Cancer 94:599-608, 2006). All the SNT cells exhibits common rearrangement of Vγ9-JγP and Jδ3 genes. The γ-δ T-cells obtained from healthy volunteers were expanded ex vivo by 1 µM of zoledronate (ZOL) plus IL-2 for 14 days incubation. Global gene expression was analyzed using the Affymetrix Human Genome U133 2.0 Plus GeneChip Set. Analysis of variance (ANOVA) was done using GeneSifter ® (VizXLabs). Values of p
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haematologica the hematology journa
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Information for readers, authors an
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EHA Executive Board E. Hellström-L
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Poster session I POSTER SESSION POS
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12 th Congress of the European Hema
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dasatinib. Methods. We studied Ikar
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Expression of the oncogene H-Ras an
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is the gene for the erythropoietin
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safety of a slow-release liposomal
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0029 OUTCOME OF THE TREATMENT OF AD
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drug-induced apoptotic response of
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41% in the PI3K- group (p=0.001). I
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Acute myeloid leukemia - Clinical I
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to 60 years (n=116, or 72%) receive
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0056 PROGNOSTIC SIGNIFICANCE OF FLT
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Anemia and Bone marrow failure 0061
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tified with the current protocol. S
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new cases of lead poisoning due to
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icance, from baseline to week 6 (p
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0086 THROMBELASTOGRAPHIC CHART RELI
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trials. The aim of this retrospecti
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tant function in this disease, nega
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ed to a favorable outcome. Bialleli
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stronger levels of p21 in the cell
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hematological centers in one countr
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ure 1). Conclusions. Results for re
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patients. After a median follow-up
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Cytogenetics and Molecular diagnost
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0135 ROUTINE DETECTION OF CYTOGENET
Page 59 and 60: (MMolR, defined as a BCR-ABL x 100
Page 61 and 62: 0146 ARSENIC TRIOXIDE INDUCES ACCUM
Page 63 and 64: tinguish between genotypic B-cell l
Page 65 and 66: Genomics and proteomics 0158 PLASMA
Page 67 and 68: 0164 EVALUATION OF MULTIPLEX LIGATI
Page 69 and 70: each patient’s replicate conditio
Page 71 and 72: 0174 RELATION BETWEEN LOW PML-RARα
Page 73 and 74: 0179 ESHAP VS GIN AS SALVAGE AND MO
Page 75 and 76: Immunology and gene therapy 0184 EA
Page 77 and 78: Cell viability was not affected by
Page 79 and 80: month is not relevant to chronic Gv
Page 81 and 82: Infection and supportive care I 020
Page 83 and 84: 0206 POTENTIAL ROLE OF CMV IN THE O
Page 85 and 86: 3H-thymidine uptake in cell culture
Page 87 and 88: 0217 TUBERCULOSIS AMONG A COHORT OF
Page 89 and 90: 0222 COMPARISON OF IWG 2006 AND IWG
Page 91 and 92: tem (IPSS) to h-MDS was also invest
Page 93 and 94: PCH97-19) were studied. Conventiona
Page 95 and 96: of erythroid colonies was reduced i
Page 97 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: itating tumor development, or engag
Page 113 and 114: usage (2/20 ie 10%) were observed.
Page 115 and 116: 0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
Page 117 and 118: (range, 1-6) and 11 treatment cycle
Page 119 and 120: 0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
Page 121 and 122: functional activity was confirmed b
Page 123 and 124: No major toxicity, neither hematolo
Page 125 and 126: enewal potential of X-RAR-positive
Page 127 and 128: (50-99) respectively. Serial analys
Page 129 and 130: cell-interaction, adhesion and acti
Page 131 and 132: 0340 ALTERED FIBRIN CLOT STRUCTURE
Page 133 and 134: Conclusions. This study demonstrate
Page 135 and 136: 0354 FACTOR V LEIDEN HOMOZYGOUS GEN
Page 137 and 138: Results. From July 2005 through Mar
Page 139 and 140: 0364 CLINICAL EFFICACY OF OXALIPLAT
Page 141 and 142: one marrow and peripheral blood ste
Page 143 and 144: ecently suggested (Boissel et al.,
Page 145 and 146: 0378 SAFETY AND EFFICACY OF THE TER
Page 147 and 148: Cytogenetics and molecular diagnost
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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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
Page 377 and 378:
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
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
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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
Page 401 and 402:
1063 ABNORMAL METHYLATION STATUS OF
Page 403 and 404:
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
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
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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
Page 431 and 432:
characterized in 198 β thalassaemi
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
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of the drug is crucial to allow lon
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egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
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
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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
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
Page 555 and 556:
1548 QUALITY ANALYSIS OF THE MULTID
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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
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