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12 th Congress of the European Hematology Association ALL CR2(2), MDS(1), secondary MDS post AML(2), blast crisis CML(2). Most patients were heavily pre-treated and 5 had previous TBI containing transplants (3 autografts, 2 allografts). Two had significantly low transfer factor pre-transplant (DLCO less than 60% predicted) and two patients had previous confirmed invasive fungal infections. The donors were 4 matched sibling, 1 mismatched sibling and 7 matched unrelated with PBSC used in 9 transplants; median CD34 dose 6.8 ×10 6 CD34/kg (range 1.17 to 11.48) and BM in 3; median mononuclear dose 3.25 × 10 8 mononuclear cells/kg (range 2.65 to 4.32). Results. Toxicities were limited with maximum Grade II mucositis and no patient required continuous opiate infusion. Renal and hepatic toxicity was minimal and thought to be unrelated to the regimen. There were no cases of VOD. The median length of stay was 42 days (range 23 to 50). 11/12 patients engrafted (1 developed RSV at Day +10 and subsequently died) with median time to platelet recovery >20×10 9 /L Day +13, >50 ×10 9 /L Day +17, neutrophils >0.5×10 6 /L Day +19, >1×10 6 /L Day +21. One patient developed acute graft rejection within 100 days. Two patients had evidence of mixed lymphoid chimerism. One has received DLI with resolution and neither has relapsed. The incidence of acute GVHD was low with only Grade 1 skin involvement in 4 patients. One patient has developed severe extensive chronic GvHD requiring long term immunosuppression. Three patients have relapsed and 2 have died, the third remains alive in remission with extensive chronic GVHD four years after DLI. The non-relapse mortality at D100 was 8% (1/12) with an overall survival at 1 year of 75%. The regimen has been well tolerated with a mean Karnovsky score at Day 100 of 70% and at 1 year 90%. Conclusions. We found this conditioning regimen to be well tolerated with acceptable levels of toxicity in high risk patients without compromising engraftment or increasing relapse rates to unacceptable levels. We suggest consideration of this regimen for patients who are at high risk of relapse and for whom a TBI containing myeloablative regimen is unsuitable due to co-morbidity or previous radiotherapy. 1249 OCCURRENCE OF EBV INDUCED B CELLS LYMPHOMA IN TWO PATIENTS TREATED CONCOMITANTLY WITH FLUDARABINE, CYCLOPHOSPHAMIDE AND ALEMTUZUMAB S. Rigaudeau, 1 C. Copie-Bergman, 2 F. Boidart, 1 I. Garcia, 1 A.L. Taksin, 1 M. Harzic, 1 S. Ghez, 1 F. Merabet, 1 P. Rousselot, 1 P. Gaulard, 2 S. Castaigne1 1 2 CHV André Mignot, LE CHESNAY, France; Hopital Henri Mondor, CRÉTEIL, France Because of strong immunosuppression, Epstein Barr Virus (EBV) positive lymphoproliferative disorders (LPD) are frequently observed in HIV patients or after transplantation. EBV+ LPD have been reported after treatment of low-grade lymphomas or chronic lymphocytic leukaemia (CLL) with Fludarabine. We report here two cases of an EBV+ LPD occurring after the use of Fludarabine, Cyclophosphamide and Alemtuzumab. A 68 year-old man had a diagnosis of B CLL (Matutes score 4/5) with a del 11 q on conventional cytogenetic analysis of peripheral blood lymphocytes. He was treated with 5 courses of oral Fludarabine (50 mg/day D1-D3) and Cyclophosphamide (400 mg/day D1-D3) from September 2003 to February 2004 with good response. He relapsed in April 2006 with multiple peripheral lymph nodes and splenomegaly. Cytological examination of lymph nodes showed features of CLL with no large cells. Total lymphocytes count was 1090/mm 3 . He received 9 weekly subcutaneous injections of Alemtuzumab (30 mg/injection). In June 2006, erythroblastopenia and acute hepatitis occurred and a parvovirus B19 infection was diagnosed. He received intravenous immunoglobulins. Treatment with Alemtuzumab was stopped. In January 2007, high fever, abdominal pain, night sweats and blood analysis consistent with an haemophagocytic syndrome appeared. Computed tomographic scan showed hepatosplenomegaly and multiple abdominal enlarged lymph nodes . The detection of EBV by PCR analysis was positive in the serum. A lymph node biopsy showed features of EBV + CD20 + Hodgkin-like lymphoproliferative disorder consistent with the diagnosis of EBV induced B cell lymphoma. The patient is now treated with Rituximab and CHVP with a good response. A 68 year-old man had in 2004 a diagnosis of T prolymphocytic leukaemia without clinical symptoms nor tumoral syndrome. He was untreated until 2005 when he was referred to our center with major asthenia, hepato-splenomegaly, pleural effusion and ascitis; total lymphocytes count was 108 000/mm 3 . Immunophenotype revealed T lymphocytes CD3 + CD4 + CD52 + . A course of CHOP was unsuccessful and treatment with oral Fludarabine (50 mg/d D1-D3), oral Cyclophosphamide (600 mg/d D1-D3) and Alemtuzumab (30 mg/injection) was started in February 2006. He received a total of 8 monthly courses of Fludarabine and Cyclophosphamide and 454 | haematologica/the hematology journal | 2007; 92(s1) Alemtuzumab by subcutaneous injections at a dose of 30 mg times 3 weekly for 4 months, then once per month for 6 months. In December 2006 he noted an enlarged cervical lymph node. Fever, night sweats, and serum analysis were consistent with an hemophagocytic syndrome. Histological examination of the cervical lymph node showed features of EBV+ diffuse large B cell lymphoma consistent with the diagnosis of EBV induced B cell lymphoma. The patient is currently treated with Rituximab and CHOP. These two cases are different by the initial pathology and the way of administration of Fludarabine, Cyclophosphamide and Alemtuzumab. Nevertheless they emphasize the risk of EBV induced lymphoma in severe immunodeficient patients. The concomitant use of three immunosuppressive agents must be weighted carefully. The monitoring of EBV viral load in serum should be performed routinely as is done the measure of cytomegalovirus viral load . 1250 FROM STEM CELLS TO CIRCULATING BLOOD: DYNAMIC AND ARCHITECTURAL ASPECTS OF HEMATOPOIESIS D. Dingli, 1 A. Traulsen, 2 J.M. Pacheco3 1 Mayo Clinic, ROCHESTER, USA; 2 Harvard University, CAMBRIDGE, USA; 3 University of Lisbon, LISBON, Portugal Background. Circulating blood cells undergo continuous cell turnover and are constantly being produced within the bone marrow in the process of hematopoiesis. At the root of blood cell formation are the hematopoietic stem cells (HSC). Recently, it was shown that the size of the active HSC pool is small (~400 cells in adult humans) and these cells replicate at a very slow rate (~1/year). In contrast, the average marrow output of ~ cells per day in huge. To date, no simple model has been able to capture the essential features of the scaling in time and population that characterize hematopoiesis. Aims. To develop a testable model that can account for the amplification and differentiation of blood cell formation over such a wide range of time scales. Methods. We consider that hematopoiesis is divided into compartments where cells in any compartment i divide to produce 2 daughter cells. The two cells either differentiate (with probability ?) and move to the next compartment (i+1) or, with probability (1-?), remain in compartment i for amplification of that compartment. Cells lost from compartment i, are replaced by cells from compartment i-1 so that the population within each compartment remains constant under stationary conditions. We utilize data from granulocyte production to calibrate the model. Results. Our model predicts that there are at least 31 amplification and differentiation steps between the active HSC pool and circulating blood cells. In any given compartment, meaning that in general, cells in any compartment differentiate and move to the next compartment downstream rather than self-renew. The model predicts the size and the replication rate of cells within any compartment. When tested on the limited data available for PIG-A mutant cells in the circulation, the model accurately predicted the average life duration of these clones in healthy adults. Summary/Conclusions. Hematopoiesis can be visualized as a series of cell filled compartments where amplification and differentiation occur. Blood production is due to an exponential increase in the number of cells due to increasingly rapid replication rates as differentiation occurs. The model makes predictions that agree closely with the limited data available in the literature. The model can be utilized to gain insights into various hematopoietic disorders and such studies are underway. 1251 HIGH SERUM FERRITIN LEVEL IS AN IMPORTANT PREDICTIVE FACTOR FOR POOR STEM CELL MOBILIZATION IN PATIENTS WITH HEMATOLOGIC MALIGNANCIES M. Yoo Hong, H.W. Lee, I.H. Park, S.H. Yoon, S.J. Kim, D.Y. Hwang, Y.R. Kim, J.S. Kim, J.W. Cheong Yonsei University College of Medicine, SEOUL, South-Korea Background. Iron overload presented by high level of serum ferritin is often observed in various hematologic diseases. Iron overload has some negative effect on engraftment and survival after hematopoietic stem cell transplantation. Aims. We analyzed the effect of transfusional iron overload in patients with hematologic malignancy on mobilization of CD34 + cells. Methods. We evaluated 50 patients, 18 (36%) with multiple myeloma, 25 (50%) with malignant lymphoma and 7 (14%) with AML. Median duration from diagnosis to stem cell collection is 166 days (range, 27 - 484 days) and mean number of packed RBC transfusion is 4.8 unit (range, 0 - 20 units). Iron overload is defined that serum ferritin level is >1000 ng/mL. The patients with non-transfusional hyperferritinemia were excluded. Results. Fifteen patients (30%) were considered iron over-
loaded group and 35 (70%) were non-iron overloaded group. Mean serum ferritin level was 2,432 ng/mL in iron overloaded group and 678ng/mL in non-iron overloaded group (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
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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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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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BRIC 126 and 4N1K) in cells lacking
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sclerosis[NS] and 12 Mixed cellular
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0927 MK-0457, A NOVEL MULTIKINASE I
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Publication Only 0933 CLINICAL FEAT
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HSCT from the available Asian as we
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that the incidence of JAK2 mutation
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without type 2 diabetes. Methods. T
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pts (38.8%) that were isolated (abs
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y using the Miltenyi CD34 isolation
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0969 COMPARISON OF CD25 IMMUNOHISTO
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cytes was 24 days (range 8-32 days)
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a cytogenetic hallmark for M4/M5 su
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normal human BM B progenitor cells
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0994 INCIDENCE OF INVASIVE ASPERGIL
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3 of disease relapse.TRM at day+100
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survival of five years. This dismal
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1011 FLOW CYTOMETRIC DNA INDEX AND
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1018 THE EFFECT OF THE SUGARBAKER P
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1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
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1063 ABNORMAL METHYLATION STATUS OF
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1069 CLINICAL RELEVANCE OF REGULATO
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1076 SERUM LEVELS OF SOLUBLE HLA CL
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patient is still undergoing intensi
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nificant MVD differences were detec
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: treatment of acute promyelocityc le
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
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acute leukemia. However, we cannot
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agents. They involve primarily the
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voriconazole for 2 months followed
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typed using a commercially availabl
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low up of ABL KD mutations’ level
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with development of BC/AP. 2. EVI-1
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1447 THE IMPACT OF DISPARITY IN SHO
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three had visual field defects, two
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acquired mutation most prone to cau
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1466 ROS GENERATION AND APOPTOSIS I
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1473 DIARRHEIC SYNDROME, A CLINICAL
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gene fusion is an independent progn
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1484 EPIDEMIOLOGY AND RESPONSE TO T
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1492 FREQUENCY OF MEDITERRANEAN GLU
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immune globulin was administered at
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maintained on Imatinib 400 mg. Afte
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Hodgkin’s disease is well known,
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gram provided a unique chance to de
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even when ADP-induced plt activatio
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medullary involvement of multiple m
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1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
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Bahr, J., 0148 Bai, M., 1551 Baia,
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Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
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El-Sharkawy, N., 0016 Elwahidi, G.,
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Garcia-Frade, J., 0346, 0680, 1105
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H Haas, N., 0742 Haas, O.A., 0001,
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Jaksic, B., 0127, 0446 Jaksic, O.,
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Körmöczi, G., 0848 Kornblau, S.,
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Lin, L.-I., 0030, 0484 Lin, T., 012
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Massé, A., 0249 Massó, P., 1287,
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Musto, P., 0254, 0401, 0422, 0569,
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Papadavid, E., 1442 Papageorgiou, E
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Probatova, N., 0704 Prochazka, V.,
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Rykavicin, O., 0504 Ryningen, A., 0
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Sirard, C., 0127, 0128 Sirigou, A.,
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Thiebaut, A., 0454 Thieblemont, C.,
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Vincenzi, C., 1060 Viniou, N.-A., 0
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Zouabi, H., 0503, 0999 Zoumbos, N.C
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12th Congress of the European Hematology ... - Haematologica

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