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12 th Congress of the European Hematology Association quantitative PCR, MRD is also detectable and measurable in peripheral blood (PB) of AML patients. Aims. Based on these premises, we assessed by MPFC the levels of MRD in PB and BM samples of 55 adult patients with AML to verify the feasibility of MRD detection in PB and its prognostic relevance. Methods. A total of 55 adult patients with AML were entered into the EORTC/GIMEMA protocols AML10/AML12 (age 61 yrs), consisting in intensive induction and consolidation cycles, and, for patients aged
0497 SINGLE AGENT CLORETAZINE (VNP40101M) IN ELDERLY AML PATIENTS WITH UNFAVORABLE CYTOGENETICS: RESULTS FROM A PHASE II MULTI-CENTER STUDY N. Vey, 1 D. Rizzieri, 2 J. Karp, 3 V. Karsten, 4 A. Cahill, 4 F. Gile s5 1 Paoli-Calmettes, MARSEILLE CEDEX 9, France; 2 Duke University, DURHAM, NC, USA; 3 Johns Hopkins University, BALTIMORE, MD, USA; 4 Vion Pharmaceuticals, NEW HAVEN, CT, USA; 5 UT MD Anderson Dept of Leukemia, HOUSTON, TX, USA Background. Outcomes for elderly patients with AML are poor, and it has been shown that elderly patients with unfavorable cytogenetics have a particularly poor prognosis. Additionally, a large number of these patients are considered unfit for intensive chemotherapy due to coexisting comorbidities, and are given best supportive care or low-dose AraC. However, no complete remissions are observed with this treatment and median overall survival is approximately 1 month (Burnett et al., Cancer 2007). Patients with unfavorable cytogenetics who do receive cytotoxic induction treatment achieve complete response rates between 23-33% with very low 5-year survival rates (2-4%) (Grimwade et al Blood 2001, Rowe et al Blood 2004, Farag et al Blood 2006, Buechner et al JCO 2006). Methods. We present a subset analysis of patients with unfavorable cytogenetics in a Phase II study of Cloretazine ® as a single agent (Vion Study CLI-033). Cloretazine? is a new alkylating agent that causes DNA crosslinks and cell death. The study was designed for untreated patients with AML or high-risk MDS over the age of 60. Treatment consisted of Cloretazine ® (VNP40101M) 600 mg/m 2 administered as a short IV infusion on day 1 (second cycle allowed) and an additional 400 mg/m 2 as consolidation for responders (CR or CRp). The primary endpoint was overall response (CR or CRp). Overall survival and relapse-free survival were also analyzed. Results. The study treated 128 patients of age 60 or older. Fifty-eight patients (45%) had unfavorable cytogenetics (-7, del5q, abnl11q, abnl9q, abnl20q, abnl13q, complex (≥ 3 abnormalities)). Of these 58 patients, 28 (48%) had secondary AML, 19 (33%) had de novo AML and 11 (19%) had high-risk MDS. Twenty-three (40%) patients in the unfavorable group had a complex karyotype. The response rate in patients with unfavorable cytogenetics was 26% (15/58). Response by diagnosis: 53% in de novo AML, 27% in MDS and 7% in secondary AML. Median overall survival in patients with unfavorable cytogenetics was 3 months (range 0.1-28). In patients achieving CR or CRp, median overall survival was 5 months (range 2-28) and relapse-free survival was 3.5 months (range 1-20). In non-responders, overall survival was 2 months (range 0.1-9). Twelve (21%) patients died within 30 days of receiving induction treatment. Conclusions. Cloretazine ® has the ability to induce remissions in elderly AML patients with unfavorable cytogenetics. Survival in this group is improved compared to that reported for supportive care or low dose AraC. Cloretazine ® may provide an important treatment option for poor prognosis patients with AML. 12 th Congress of the European Hematology Association Autologous stem cell transplantation 0498 THE ROLE OF HIGH DOSE CHEMOTHERAPY AND PERIPHERAL BLOOD STEM CELL SUPPORT IN REFRACTORY TROPHOBLASTIC DISEASE AND NON-GESTATIONAL CHORIOCARCINOMA: A REVIEW OF EIGHT PATIENTS I. Gabriel, 1 A. Chaidos, 1 C. Giles, 1 J. Apperley, 1 M. Seckl, 2 M. Bower, 3 E Kanfer1 1 Hammersmith Hospital NHS Trust, LONDON; 2 Charing Cross Hospital, LONDON; 3 Chelsea and Westminster Hospital, LONDON, United Kingdom Objective. To evaluate the role of high dose therapy (HDT) with autologous peripheral blood stem cell support (ASCT) refractory advanced trophoblastic disease and non gestational choriocarcinoma. Methods. Eight patients (gestational trophoblastic neoplasia n =6, choriocarcinoma post complete hydatidiform mole n=1, possible non-gestational choriocarcinoma n=1 and germ cell tumour with choriocarcinoma differentiation n=1) were treated with HDT with ASCT. Median age was 33 years. All patients received a conditioning regimen of CarboPEC-Taxol (Paclitaxel 75 mg/m 2 on days -7, -5, and -3, Etoposide 450 mg/m 2 days -7, -5, and -3, Carboplatin 10 mg x glomerular filtration rate (GFR) +25 on days -7, -5,and -3, and Cyclophosphamide 60 mg/kg/day days -5, and -3). Four patients received this regimen as a tandem ASCT, receiving 50% dose of the conditioning regimen drugs with stem cell infusion twice, twelve weeks apart, to limit toxicity. All eight patients had multiply relapsed disease and had received more than two different prior treatments (median number of prior therapies was 3.5 range, 2-5) at time of ASCT. Two patients had cerebral metastases. At transplant four patients were in a partial remission (PR) and four had progressive metastatic disease. Results. The regimen was well tolerated. Seven patients showed an initial response immediately post ASCT, one patient demonstrated disease progression throughout. Five patients achieved a complete remission (CR) demonstrated by a reduction in serum tumour markers to normal (
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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
Page 141 and 142: one marrow and peripheral blood ste
Page 143 and 144: ecently suggested (Boissel et al.,
Page 145 and 146: 0378 SAFETY AND EFFICACY OF THE TER
Page 147 and 148: Cytogenetics and molecular diagnost
Page 149 and 150: 0385 CYTOPLASMIC MUTATED NUCLEOPHOS
Page 151 and 152: 0390 ELTROMBOPAG RAISES PLATELET CO
Page 153 and 154: factor for the achievement of CR wa
Page 155 and 156: The cases of RAS showed two peaks o
Page 157 and 158: is 85%. Seven out of the 25 relapse
Page 159 and 160: 0409 FRACTIONATED RADIOIMMUNOTHERAP
Page 161 and 162: 0414 COMPARATIVE ANALYSIS OF THE CO
Page 163 and 164: successfully managed with GM-CSF di
Page 165 and 166: 49% for PCR positive patients (95%
Page 167 and 168: +8 (1 PR+1 HI) and 14/24 pts with c
Page 169 and 170: (e.g. bcr-abl leading to CML). CSC
Page 171 and 172: 0438 TERC MUTATIONS ANALYSIS IN PAT
Page 173 and 174: observed in all mice. Analysis of l
Page 175 and 176: ex-vivo expansion of HUCB-derived H
Page 177 and 178: ic kidney disease in univariate or
Page 179 and 180: One hundred eleven CN AML patients,
Page 181 and 182: to asses intestinal epithelial dama
Page 183 and 184: genesis of acute myeloid leukaemia
Page 185 and 186: polymorphism at nucleotide 4889 of
Page 187 and 188: expression along with a decreased C
Page 189 and 190: 0487 MUTATIONAL STATUS OF NUCLEOPHO
Page 191: previously reported, a single cours
Page 195 and 196: ly received melphalan-based chemoth
Page 197 and 198: were similar among the 3 groups. Ho
Page 199 and 200: Methods. Several read-out systems w
Page 201 and 202: 0518 SERUM AND CELLULAR EXPRESSION
Page 203 and 204: 0523 DNA REPAIR INHIBITION IN RESTO
Page 205 and 206: held true when BMI-1 expression was
Page 207 and 208: Ph + cells in the bone marrow). We
Page 209 and 210: derivative chromosome (4p16, 7p14,
Page 211 and 212: 0545 STABILIZED BONE MARROW IS NOT
Page 213 and 214: obtained in low (Sokal) risk patien
Page 215 and 216: median dose intensity being 800 (21
Page 217 and 218: from pivotal clinical trials. Metho
Page 219 and 220: Cytogenetics and Molecular diagnost
Page 221 and 222: to set up and optimize a D-HPLC-bas
Page 223 and 224: 0576 WESTERN BLOT IDENTIFICATION OF
Page 225 and 226: Basic disease was AML (n=5), ALL (n
Page 227 and 228: 0588 EXTRACORPOREAL PHOTOPHORESIS F
Page 229 and 230: acquire a cytolytic capacity agains
Page 231 and 232: informed vignettes describing healt
Page 233 and 234: using CHOP-21 in the UK, pegfilgras
Page 235 and 236: 0609 SOFT TISSUE COMPLICATIONS IN P
Page 237 and 238: inding lectin (MBL) gene by polymer
Page 239 and 240: all infection rate (p=0.12) as well
Page 241 and 242: 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
Page 341 and 342:
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
Page 415 and 416:
1105 CYTOGENETIC ABNORMALITIES IN 3
Page 417 and 418:
1110 CONSTITUTIVE ACTIVATION OF STA
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efficacy results with a well-tolera
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unmutated VH genes, and high and lo
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Aims. Aim of this study was to pred
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tested across a wide range of human
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were incidentally diagnosed (52%).
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ß2GP1 may be considered as determi
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characterized in 198 β thalassaemi
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
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of the drug is crucial to allow lon
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egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
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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
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posed, was: DF = (CD43%+FMC7%+CD79b
Page 461 and 462:
treatment of acute promyelocityc le
Page 463 and 464:
loaded group and 35 (70%) were non-
Page 465 and 466:
mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
Page 469 and 470:
ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
Page 475 and 476:
disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
Page 479 and 480:
phamide 750 mg/m 2 on day 1, vincri
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
Page 497 and 498:
Results. Though there was no recogn
Page 499 and 500:
2% and 19% of patients with or with
Page 501 and 502:
were older than 65 y) which can be
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
Page 505 and 506:
median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
Page 509 and 510:
to the presence of IVS1-6 mutation
Page 511 and 512:
fy predictive factors for these abn
Page 513 and 514:
acute leukemia. However, we cannot
Page 515 and 516:
agents. They involve primarily the
Page 517 and 518:
voriconazole for 2 months followed
Page 519 and 520:
typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
Page 523 and 524:
with development of BC/AP. 2. EVI-1
Page 525 and 526:
1447 THE IMPACT OF DISPARITY IN SHO
Page 527 and 528:
three had visual field defects, two
Page 529 and 530:
acquired mutation most prone to cau
Page 531 and 532:
1466 ROS GENERATION AND APOPTOSIS I
Page 533 and 534:
1473 DIARRHEIC SYNDROME, A CLINICAL
Page 535 and 536:
gene fusion is an independent progn
Page 537 and 538:
1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
Page 541 and 542:
immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
Page 545 and 546:
Hodgkin’s disease is well known,
Page 547 and 548:
gram provided a unique chance to de
Page 549 and 550:
even when ADP-induced plt activatio
Page 551 and 552:
medullary involvement of multiple m
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
Page 555 and 556:
1548 QUALITY ANALYSIS OF THE MULTID
Page 557 and 558:
Index of authors A Aapro, M., 0377,
Page 559 and 560:
Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
Page 567 and 568:
El-Sharkawy, N., 0016 Elwahidi, G.,
Page 569 and 570:
Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
Page 573 and 574:
Jaksic, B., 0127, 0446 Jaksic, O.,
Page 575 and 576:
Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
Page 581 and 582:
Musto, P., 0254, 0401, 0422, 0569,
Page 583 and 584:
Papadavid, E., 1442 Papageorgiou, E
Page 585 and 586:
Probatova, N., 0704 Prochazka, V.,
Page 587 and 588:
Rykavicin, O., 0504 Ryningen, A., 0
Page 589 and 590:
Sirard, C., 0127, 0128 Sirigou, A.,
Page 591 and 592:
Thiebaut, A., 0454 Thieblemont, C.,
Page 593 and 594:
Vincenzi, C., 1060 Viniou, N.-A., 0
Page 595 and 596:
Zouabi, H., 0503, 0999 Zoumbos, N.C
Page 597 and 598:
Page 599 and 600:
Page 601 and 602:
Page 603:
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