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12 th Congress of the European Hematology Association decreases or increases (p
Hodgkin’s disease is well known, but association with other lymphoproliferative disorders is rare. To our knowledge, this is the second case of follicular lymphoma associated with LCH. In the first case, LCH was diagnosed simultaneously with the lymphoma. By contrast, in our case, LCH was diagnosed 3 years after the lymphoproliferative disease, when there were no evidence of follicular lymphoma progression. The origin of LCH is not clear, and there is controversy as to whether it represents a true independent clonal neoplasm or a reactive and/or therapy-related phenomenon. Reviewing the literature, FDG-PET study appears to have higher sensitivity than bone scintigraphy, radiography and MR imaging for the identification of active osseous lesions in LCH. However, it also has a limited spatial resolution and requires complementary CT or MR imaging to define the area of increased glucose metabolism. In summary, FDG-PET atypical uptakes appearing in a patient with lymphoproliferative disease in complete remission should not be considered as lymphoma progression without confirmation by histologic examination. 1511 FLUDARABINE PLUS CYCLOPHOSPHAMIDE (FC) IN PATIENTS WITH PREVIOUSLY UNTREATED LOW-GRADE LYMPHOMA M. Dell’Olio, C. Bodenizza, A.M. Carella, A. Falcone, M.M. Greco, A. La Sala, S. Mantuano, L. Melillo, E. Merla, M. Nobile, G. Sanpaolo, P. Scalzulli, N. Cascavilla Casa Sollievo della Sofferenza Hosp., SAN GIOVANNI ROTONDO, Italy Background. In the last years, fludarabine alone or in combination with other drugs has been reported to be effective in the treatment of previously treated low-grade non-Hodgkin’s lymphomas (LG-NHL). The aim of this study was to define the therapeutic efficacy and toxicity of a combination of fludarabine and cyclophosphamide (FC regimen) in untreated LG-NHL. Patients and Methods. Between January 2002 and June 2006, forty-five previously untreated patients with LG-NHL, were enrolled in the study. All patients (M/F: 28/17, median age 62 years) vere treated with three-day courses of fludarabine 25 mg/m2 /day, cyclophosphamide 300 mg/m2/day, every four weeks for a maximum of six courses. Granulocyte colony-stimulating factor and Pneumocystis Carinii prophylaxis was given. Among 45 patients, 21 (46%) were diagnosed with small lymphocytic, 9 (20%) with malt gastric, 8 (18%) follicular grade I, and 7 (16%) with immunocytoma subtypes. Results. Of the 45 patients, 43 (94%) achieved complete response (CR), 1 (3%) partial response, while the remaining 1 (3%) showed no benefit from the treatment. Regarding histology, in the follicular and malt gastric subtype we observed an overall response (OR) rate and CR rate of 100%. Median duration of follow-up was more than 27 months. Overall survival and disease-free survival rates were 93% and 88%. Hematologic grade 3-4 toxicity was seen in only five (11%) patients; no opportunistic infections or deaths were associated with the administration of the FC regimen Conclusion. These preliminary data show that the FC regimen is a high level of activity, with prolonged CR, well-tolerated combination chemotherapy for untreated patients with LG-NHL. 1512 MANAGEMENT OF SEVERE MUSCULOSKELETAL PAIN CAUSED BY IMATINIBE MESYLATE WITH DULOXETINE HYDROCHLORIDE IN A PATIENT WITH CHRONIC MYELOID LEUKEMIA (CML). A CASE REPORT S. Vakalopoulou, E. Pagourelias, Z. Katsarou, V. Perifanis, S. Theodoridou, V. Garipidou Ippokration General Hosital,Thessaloniki, THESSALONIKI, Greece Imatinibe mesylate is an orally administered inhibitor of the breakpoint cluster region-Abl tyrosine kinase, which is capable of blocking proliferation and inducing apoptosis in chronic myeloid leukemia cell lines. Its introduction in everyday clinical practice led to an advantageous hematological and cytogenetic response in patients suffering from CML, even though mild or more severe adverse effects of the drug may present, affecting patients’ compliance or even calling for treatment withdrawal. We present the case of a 23 year old patient with chronic myeloid leukemia under imatinibe mesylate (Gleevec 400 mg once daily) who developed severe musculoskeletal pain located at the lower extremities (due to the above treatment) and its management with Duloxetine Hydrochloride. After the patient was diagnosed to suffer from CML (G-banding karyotype showed 46,XX,t(9;22)(q34;q11) and a BCR-ABL transcript was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) on bone marrow), a treatment with Gleevec begun. After two weeks of treatment (400 mg once daily) the patient complained for acute dysaesthesias and paraesthesias of the legs as long as for severe pain on the same area. The above symptoms had 12 th Congress of the European Hematology Association the typical distribution of an acute polyneuropathy. Despite that and the findings of the clinical examination a full laboratory investigation (including X Rays of the area, biochemical analysis and an electromyogramm) didn’t prove the existence of polyneuropathy. Because of the severity of pain the patient received large doses of paracetamol plus codeine or even dextropropoxyphene hydrochloride without satisfactory analgetic results. subsequently, duloxetine hydrochloride (Xeristar) was administered initially at doses of 30 mg once daily for the first four days and continuing with 60 mg once daily. The patient responded to the treatment. One week later she needed no more opiates while after two weeks the symptoms were fully relieved. Duloxetine Hydrochloride is a new SSRI approved by FDA both for the treatment of depression as along as for the management of diabetic polyneuropathy. As far as we know it is the first time for this drug to be used successfully in the management of acute musculoskeletal pains due to imatinibe mesylate. It is certain that prospective studies are needed to evaluate the efficacy and safety of the drug under conditions similar to the above. However, duloxetine hydrochloride offers a new alternative choise for pain alleviation in patients receiving Gleevec which seems to be much more attractive than treatment withdrawal. 1513 GRAFT VERSUS HOST DISEASE AFTER ALLOGENEIC STEM CELL TRANSPLANTATION AND ITS PREDICTION BY PROTEOMIC APPROACHES A.K. Kaplanova Department of Hematooncology, BRNO, Czech Republic Background. Acute graft-versus-host disease (GvHD) is a frequent complication of allogeneic stem cells transplantation (allo-SCT). The rapid diagnosis of acute GvHD following allo-SCT is important for optimizing the management of this life-threatening complication. Differentially expressed or excreted polypeptides and proteins have potential for early and accurate diagnosis of GvHD and other complications of allo-SCT. Aims. Search for blood plasma proteins useful as potential biomarkers for early detection of GvHD. Methods. 2-dimensional gel electrophoresis (2- DE) was used for separation of blood plasma proteins. Proteins considered as potential biomarkers for early prediction of GvHD were selected by image analysis. Protein spots with different expression levels were characterized by matrix-assisted laser desorption/ionization - time of flight mass spectrometry (MALDI-TOF-MS) using peptide mass fingerprinting. Samples of blood plasma, urine and lymphocytes, collected from the same patient before and after allo-SCT were analyzed. Analysed samples were collected at three time points: (1) approx. 10 days before GvHD manifestation, (2) approx. 2 days before GvDH manifestation and (3) during GvHD manifestation. Results. Proteomic analysis revealed several proteins differentially expressed during GvHD development. These potential biomarkers included serum natural proteinases (macroglobulin α2 and α1 anti-trypsin), components of complement (complement 4 binding protein and complement factor I), proteins of acute phase (haptoglobin, C-reactive protein and amyloid related serum protein (SAA)) and other proteins such as fibrin, fibrinogen, inter-α (globulin) inhibitor H4 and hemopexin precursor. Concentration of serum natural proteinases, haptoglobin, inter-α (globulin) inhibitor H4 and hemopexin precursor in blood plasma were significantly decreased in both samples collected prior to GvHD manifestation. In these samples was detected also slightly decreased expression of analyzed components of complement in comparison to samples collected during GvHD manifestation. On the other hand, expression of C-reactive protein and SAA was detected only 14 days before GvHD manifestation and these proteins completely disappeared 1 day before onset of disease and during its manifestation. Summary/Conclusions. These potential biomarkers could improve early prediction and treatment of GvHD and thereby reduce GvHD incidence and complications. This study was supported by several grant projects: IGA MZ CR NR8448- 3/205 and NR9293-3/2007, and grant projects of Ministry of Education, Youth and Sports: MSM0021622430, MSM0021624215 and LC 06034. 1514 HER-2/NEU MRNA IN PERIPHERAL BLOOD & BONE MARROW IN FEMALE BREAST CANCER PATIENTS A. Abd El Hamid, 1 M. Elkamash, 1 G. Eskander, 1 A. Hassan, 1 F. Abdel aziz, 1 F. Attia, 1 S. Hassan, 2 M. Hassan2 1 Suez Canal Univers, Faculty of Medicine, ISMAILIA,EGYPT, Egypt; 2 Karolinska University Hospital, STOCKHOLM, Sweden Background. The prognostic significance of the bone marrow haematologica/the hematology journal | 2007; 92(s1) | 537
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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
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dictor of OS (p=0.004). High dose t
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1099 ALTERATIONS IN THE NATURAL KIL
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1105 CYTOGENETIC ABNORMALITIES IN 3
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1110 CONSTITUTIVE ACTIVATION OF STA
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efficacy results with a well-tolera
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unmutated VH genes, and high and lo
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Aims. Aim of this study was to pred
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tested across a wide range of human
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were incidentally diagnosed (52%).
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ß2GP1 may be considered as determi
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characterized in 198 β thalassaemi
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1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
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of the drug is crucial to allow lon
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egarding cost analysis of ASCT in G
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ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
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events -Postoperative states: 9,19%
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efficacy and decreased atherosclero
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1217 INCIDENCE OF EARLY STAGE IDIOP
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1691GA and 1 homozygous 1691AA. The
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1230 ASSOCIATION OF HEPARANASE GENE
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posed, was: DF = (CD43%+FMC7%+CD79b
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treatment of acute promyelocityc le
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loaded group and 35 (70%) were non-
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mild. Fas and soluble Fas ligand le
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1265 POSACONAZOLE THERAPY IN REFRAC
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ly express the cytoplasmic (inactiv
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findings confirmed the significant
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a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
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1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
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phamide 750 mg/m 2 on day 1, vincri
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nomenon is unclear. It has been sug
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oped mild thrombocytopenia (platele
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gle dose of 54mg/m 2 rituximab furt
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patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
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(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: maintained on Imatinib 400 mg. Afte
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:
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