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12 th Congress of the European Hematology Association significant difference was found at RET vs Diagnosis in Non Responders. IL4 was significantly lower at RET (1324) vs Diagnosis (4748) (p 0.003) in Non Responders but not in Responders. Conclusions. 1.TNF-α and IFN-γ were confirmed to be over-expressed in marrow of both AD and NAD AAA patients. 2. TNF-α and IFN-γ decline more in patients Responding vs Non responding to IS. 3. Myelosuppressive cytokines remain in the marrow also of patients who respond to IS. This smouldering activity may contribute to relapse in case of immune attack reactivation. 4. The reduced expression of IL-4 in may contribute to the disease by not counterbalancing the Th1 polarization in Non Responding patients. Overall these data indicate TNF-α and IFN-γ as crucial effectors of marrow damage in AAA and suggest to strengthen IS with targeted anti cytokine treatments that may reduce the risk of relapse after IS. 0077 HIGH PREVALENCE OF ANAEMIA AMONG FRENCH HOSPITALIZED CANCER PATIENTS: A ONE-DAY CROSS-SECTIONAL SURVEY S. Castaigne, 1 J.M. Tourani, 2 S. Delaloge, 3 C. Hennequin, 4 M. Zureik, 5 E. Lemarié6 1 Hôpital de Versailles, LE CHESNAY; 2 Hôpital La Miletrie, POITIERS; 3 Institut Gustave Roussy, VILLEJUIF; 4 Hôpital Saint Louis, PARIS; 5 INSERM U700, PARIS; 6 Hôpital Bretonneau, TOURS, France Objective. To evaluate the prevalence of anaemia (haemoglobin [Hb] 24 hours. 76.9% of patients received cancer treatment (recurrent disease: 44.2%); 42.7% of patients had a performance status of ?2. 23.8% of patients had haematological malignancies (including lymphoma, 8.9%; and acute leukaemia, 6.3%) and 76.2% had solid tumours (including lung cancer 15.9%; colorectal cancer 14.4%; and breast cancer 12.8%). 57.6% of solid tumours were metastatic. Hb levels ranged from a minimum of 4.2 to a maximum of 18.9 g/dL (11.2±1.9). 63.8% of patients had anaemia (77.3% among patients with haematological tumours; 59.5% in patients with solid tumours). 57.8% of anaemia cases were considered to be related to cancer treatment. 59.1% of patients receiving CT were anaemic. 47.4% of anaemic patients were not being treated for their anaemia. Among patients receiving 1 or more treatment for anaemia, the treatments included transfusion (28.5%), erythropoietin stimulating protein (27.0%), and nutritional supplements (iron and/or vitamins) (19.1%). Further analysis of patients not treated for anaemia is underway. Conclusions. These results confirm the findings of ECAS, a large European survey of anaemia in cancer patients. Better identification of the causes of anaemia in cancer patients may optimize patient care. Detailed data on haematological patients will be presented. 0078 INTRAVENOUS IRON IMPROVES RESPONSE RATES TO RECOMBINANT HUMAN ERY- THROPOIETIN IN ANAEMIC PATIENTS WITH HAEMATOLOGICAL MALIGNANCY ON CHEMOTHERAPY WHICH IRON PARAMETERS TO USE? P. Greaves, 1 S. Agrawal, 1 C. Lim, 1 C. Poole2 1 2 St Bartholomew's Hospital, LONDON; Threesixtydegree Research Ltd, CARDIFF, United Kingdom Background. Recombinant human erythropoietin (rhEpo) may be used to avoid transfusion and improve quality of life in the anaemia of cancer. Poor response rates to rhEpo are a factor contributing towards its poor uptake in clinical practice. Supplementation with intravenous iron improves response rates to rhEpo. Biochemical markers of iron status may guide rational use of iron supplementation, but they are often unreliable, being altered by the same factors that disrupt iron metabolism and contribute to the anaemia of malignancy. Functional iron deficiency (FID) is a status whereby iron stores are adequate by biochemical param- 28 | haematologica/the hematology journal | 2007; 92(s1) eters but rendered inaccessible to erythropoiesis, perhaps through cytokine dysregulation. Aims. ASH/ASCO-based guidelines and a protocol-based approach to the use of intravenous iron and rhEpo in the treatment of non-myeloid haematological malignancy have been used in our centre for the last 4 years. Monitoring of several biochemical iron status markers was integral to the protocol. The aim was to determine which iron parameters most consistently predicted FID and hence the need for intravenous iron. Methods. A prospective audit was carried out of patients with non-myeloid haematological malignancy on chemotherapy and who were anaemic and receiving rhEpo. Intravenous iron supplementation was based on the following iron parameters: haemoglobin, mean corpuscular haemoglobin, serum ferritin, transferrin saturation, zinc protoporphyrin (ZPP), reticulocyte count and reticulocyte haemoglobin concentration (CHr). Measurements were made at baseline, weeks 4 and 8, then as indicated by a suboptimal haemoglobin (Hb) response. The data were examined to determine which measures most frequently triggered the addition of intravenous iron at baseline (indicating FID) and which measures most frequently indicated the development of FID during rhEpo therapy, leading to later addition of intravenous iron. Results. The iron status indices of 54 patients receiving rhEpo were analysed. 68% had myeloma, 17% CLL, 6% Waldenstrom’s macroglobulinemia and 9% other non-Hodgkin’s lymphoma. Their mean baseline haemoglobin was 9.2 g/dL. 50% of patients received intravenous iron. Abnormal baseline ZPP was most frequently the irondeficiency trigger for commencing intravenous iron supplementation on first instigating rhEpo therapy. In patients started on rhEpo alone, the development of functional iron-deficiency during rhEpo-driven erythropoiesis was best monitored by changes in transferrin saturation and serum ferritin, leading to commencement of intravenous iron. However, in some patients, intravenous iron was instituted in spite of biochemical parameters not themselves indicating iron deficiency, because of downward trends in transferrin saturation and serum ferritin. Intravenous iron commencement enabled rhEpo maintenance doses to be reduced and even discontinued. With this approach, the overall response rate was 90% (81% > 2g/dL Hb increase) and mean Hb increment was 3.25 g/dL. Summary and Conclusions. Rational use of intravenous iron to support rhEpo therapy in haematological malignancy is possible with readily available, inexpensive biochemical parameters of iron status. ZPP most frequently reflects initial iron depletion, while transferrin saturation and serum ferritin trends best reflect development of functional iron deficiency during rhEpo therapy. 0079 SEQUENTIAL MONITORING OF ERYTHROCYTE HEMOGLOBINIZATION AND IRON MARKERS DURING R-HUEPO THERAPY IN ANEMIC PATIENTS WITH MULTIPLE MYELOMA AND LYMPHOMA E.K. Katodritou, 1 E. Verrou, 1 D. Kapetanos, 1 A. Banti, 1 C. Kartsios, 1 D. Mihou, 1 V. Gastari, 1 D. Markala, 1 S. Effraimidou, 1 A. Lazaridou, 1 E. Terpos, 2 K. Zervas1 1 2 Theagenion Cancer Center, THESSALONIKI; 251 General Airforce Hospital, ATHENS, Greece Background. Recombinant human erythropoietin (r-HuEPO) stimulates erythropoiesis and increases iron demands in the erythroid marrow leading to functional iron deficiency (FID). The development of FID is an important cause of r-huEPO unresponsiveness in anemic patients with multiple myeloma (MM) and lymphoma. Close monitoring of sensitive markers of erythrocyte hemoglobinization and iron status are useful in recognizing FID early in the course of r-huEPO treatment. Aims. The aim of this study was to monitor the sequential alterations in erythrocyte hemoglobinization (EH) and iron markers in order to recognize the development of FID early in the course of r-huEPO treatment, in anemic patients with MM and lymphoma. Methods. Fourty-one patients with a median age of 71 years (range 18-84) with symptomatic MM or lymphoma and disease related anemia, were enrolled. All patients received epoietin β at a dose of 30.000IU/wk for 6 consecutive weeks. The evaluated parameters of iron status and EH, were: serum ferritin, transferrin saturation (TSAT%), soluble transferrin receptor (sTfR), the ratio of sTfR to the logarithm of ferritin (sTfR-F index), the percentage of hypochromic erythrocytes (HYPO%) and reticulocyte haemoglobin content (CHr). These parameters were evaluated in serial measurements at baseline and on weeks 1, 2 and 6. The gradual development of FID during sequential weeks was indicated by an increase in HYPO% and sTfR-F index and a reduction in CHr and TSAT%. Statistical analysis was performed with paired samples Wilcoxon test and correlations with the Spearman’s test. Results. HYPO% and sTfR-F index gradually increased during all sequential measurements showing statistical signif-
icance, from baseline to week 6 (p
Page 1 and 2: haematologica the hematology journa
Page 3 and 4: Information for readers, authors an
Page 5 and 6: EHA Executive Board E. Hellström-L
Page 7 and 8: Poster session I POSTER SESSION POS
Page 9 and 10: 12 th Congress of the European Hema
Page 11 and 12: dasatinib. Methods. We studied Ikar
Page 13 and 14: Expression of the oncogene H-Ras an
Page 15 and 16: is the gene for the erythropoietin
Page 17 and 18: safety of a slow-release liposomal
Page 19 and 20: 0029 OUTCOME OF THE TREATMENT OF AD
Page 21 and 22: drug-induced apoptotic response of
Page 23 and 24: 41% in the PI3K- group (p=0.001). I
Page 25 and 26: Acute myeloid leukemia - Clinical I
Page 27 and 28: to 60 years (n=116, or 72%) receive
Page 29 and 30: 0056 PROGNOSTIC SIGNIFICANCE OF FLT
Page 31 and 32: Anemia and Bone marrow failure 0061
Page 33 and 34: tified with the current protocol. S
Page 35: new cases of lead poisoning due to
Page 39 and 40: 0086 THROMBELASTOGRAPHIC CHART RELI
Page 41 and 42: trials. The aim of this retrospecti
Page 43 and 44: tant function in this disease, nega
Page 45 and 46: ed to a favorable outcome. Bialleli
Page 47 and 48: stronger levels of p21 in the cell
Page 49 and 50: hematological centers in one countr
Page 51 and 52: ure 1). Conclusions. Results for re
Page 53 and 54: patients. After a median follow-up
Page 55 and 56: Cytogenetics and Molecular diagnost
Page 57 and 58: 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
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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
Page 113 and 114:
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
Page 317 and 318:
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
Page 351 and 352:
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
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
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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
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1105 CYTOGENETIC ABNORMALITIES IN 3
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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
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were incidentally diagnosed (52%).
Page 429 and 430:
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
Page 441 and 442:
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
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events -Postoperative states: 9,19%
Page 451 and 452:
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
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
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ly express the cytoplasmic (inactiv
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findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
Page 477 and 478:
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
Page 487 and 488:
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
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Results. Though there was no recogn
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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
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to the presence of IVS1-6 mutation
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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,
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
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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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12 th Congress of the European Hema
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