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12 th Congress of the European Hematology Association AML1 gene point mutation. We hypothesize that LOH/DNA loss at 5q and/or 7 constitutes an important genetic mechanism involved in leukemogenesis following accidental radiation exposure. The higher prevalence of multiple ITD alleles in radiation-associated AML cases with FLT3 mutations may reflect an underlying radiation-induced genetic instability. Funded by EU contract FI6R-012964 0038 INHIBITION OF SDF-1/CXCR4 AXIS AFFECTS SURVIVAL AND DIFFERENTIATION OF HUMAN AML CELLS S. Tavor, 1 M. Eisenbach, 2 J. Jacob-Hirsch, 3 S. Kay, 2 S. Baron, 2 K. Ben-Zion, 2 N. Amariglio, 3 V. Deutsch, 2 E. Naparstek, 2 G. Rechavi3 1 Sourasky Medical Center, TEL-AVIV, Israel; 2 Department of Hematology and BMT, Tel Av, TEL AVIV, Israel; 3 Cancer Research Center, Sheba M.C., Tel-, RAMAT-GAN, Israel A number of recent studies showed that the chemokine stromal cellderived factor-1 (SDF-1) and its receptor CXCR4 participate in the retention of human acute myeloid leukemic (AML) cells within the bone marrow (BM) microenvironment, and their release into the circulation. We have also showed that AML cells constitutively express and secrete SDF- 1 dependent cell surface elastase, which regulates their migration and proliferation. To elucidate the molecular events and genes regulated by SDF-1/CXCR4 axis and elastase in AML cells, we examined gene expression of U937 AML cell line treated with neutralizing anti-CXCR4 or elastase inhibitor (EI) compared to untreated cells, using DNA microarray technology. Unsupervised hierarchical clustering analysis showed very similar gene expression profiles of anti CXCR4 mAb and EI treated cells, both differ significantly from the untreated control. 230 of the 8400 genes investigated were repressed, and 164 were induced after culturing AML cells in the presence of anti CXCR4 mAb or EI compared to untreated cells. Inhibition of CXCR4 or elastase was accompanied by down regulation of the transcripts of primary granule proteins. Functional classification of SDF-1/CXCR4 axis or elastase regulated genes revealed down-regulation of HOXA9, HOXA10, ETS2, as well as other transcription factors that are over expressed in AML, and are important for the development of leukemia. In contrast, transcriptional factors and regulators known to be induced during myeloid differentiation like C/EBPα, ID1, RUNX3 and HHEX were up-regulated in the treated cells. In addition, interleukin receptors, growth factors (G-CSFR and GM- CSF), complement component (C1QR1) were up-regulated in the treated cells. These data were confirmed by real time PCR for selected marker genes of myeloid cells differentiation. Interestingly, many of the differentially expressed genes were common to the transcriptional program of normal terminal granulocytic differentiation (Theilgaard- Monch & Borregarrd 2005. Blood 105:1785), suggesting that inhibition of SDF- 1/CXCR4 axis may induce myeloid differentiation in AML cells. We further analyzed the effect of CXCR4 pathway inhibition on AML cell differentiation and growth. Treatment of AML cell lines with the SDF- 1 antagonist AMD3100 triggered a proliferative arrest and mimicked myeloid differentiation, including morphologic changes and increased expression of myeloid differentiation antigens. In summary, our study showed that inhibition of SDF-1/CXCR4 axis or elastase in AML cells affects similar pathways related to differentiation and malignant transformation, implying a critical role for those molecules in regulating leukemic development. Repression of SDF-1/CXCR4 decreases survival and induces differentiation of AML cells, suggesting a potential new therapeutic approach for AML. 0039 RETROVIRAL INSERTIONAL MUTAGENESIS SCREEN IN A C/EBPALPHA PROLIFERATIVE GENETIC BACKGROUND M.S. Hasemann, 1 A.B. Sorensen, 2 F.S. Pedersen, 2 C. Nerlov, 3 B.T. Porse1 1 Copenhagen University Hospital, COPENHAGEN O, Denmark; 2 University of Aarhus, AARHUS, Denmark; 3 EMBL, MONTEROTONDO, Italy The CCAAT enhancer binding protein α (C/EBPα) transcription factor plays a key role in the regulation of growth and differentiation of the granulocytic lineage in the hematopoietic system and CEBPA (encoding C/EBPα) is often mutated or deregulated in AML patients. Consistently, mice lacking C/EBPα have no mature neutrophils and die within a few hours. However, homozygous knockin mice in which wild type Cebpa has been replaced with a mutant allele (BRM2), which abolish the growth-repressing ability of C/EBPα, are viable, but at 8 weeks of age 14 | haematologica/the hematology journal | 2007; 92(s1) they display myeloid dysplasia with absence of neutrophil granulocytes. Strikingly, in older CebpaBRM2/ BRM2 knockin mice the myeloid dysplastic phenotype progress into other myeloid malignancies such as myeloid proliferative syndrome and acute myeloid leukemia-like malignancy. This strongly suggests that secondary mutations in other loci must occur when developing leukemia in the CebpaBRM2/BRM2. In order to identify genes that cooperate with Cebpa mutations in the development of leukemia in CebpaBRM2/BRM2 mice a so-called retroviral insertion mutagenesis screen was performed. Inbred newborn CebpaBRM2/BRM2 and wildtype mice were injected with SRS19-6 retrovirus, which incorporated into the genome and resulted in activation of oncogenes and leukemic progression. When leukemia was evident the mice were euthanized and analyzed. As expected the CebpaBRM2/ BRM2 mice had a shorter latency than wildtype mice (186 vs. 276 days). The mice had enlarged spleen, thymus, and/or lymph nodes and were thoroughly investigated by histology, flow cytometry and southern in order to determine the leukemic phenotypes. Most of the CebpaBRM2/BRM2 mice developed an AML-like phenotype, whereas T cell leukemias were most prominent in wildtype mice, showing that mutating Cebpa specifically directs leukemic progression towards a myeloid direction. Finally, the retroviral insertion loci were identified through a splinkerette-aided PCR strategy. This led to the identification of several novel putative and previously unexplored oncogenes, which might collaborate with mutated Cebpa in the development of AML. 0040 CONSTITUTIVE PI3 KINASE ACTIVATION REPRESENTS A FAVORABLE PROGNOSTIC FACTOR IN DE NOVO AML PATIENTS UNDER 60 YEARS J. Tamburini, 1 C. Elie, 2 V. Bardet, 1 N. Chapuis, 1 S. Park, 1 P. Broët, 3 P. Cornillet-Lefebvre, 4 B. Lioure, 5 V. Hugo, 4 O. Blanchet, 4 N. Ifrah, 6 F. Witz, 7 F. Dreyfus, 8 P. Mayeux, 1 C. Lacombe, 1 D. Bouscary1 1 Institut Cochin, PARIS, France; 2 Departement de Biostatistiques, PARIS, France, 3 Faculté de Médecine Paris Sud, PARIS, France; 4 Laboratoire d'hématologie CHU, REIMS, France; 5 Departement d'hématologie CHU, STRASBOURG, France; 6 Service des Maladies du Sang CHU, ANGERS, France; 7 Service d'hématologie Hopital Brabois, NANCY, France; 8 Service d'hématologie Hopital Cochin, PARIS, France Background. Abnormal activation of kinases may promote leukemogenesis by conferring cell proliferation and survival advantage in acute myeloid leukemia (AML). New targeted therapies are currently developed to disrupt such activation, to improve the long term prognosis of AML patients. However, the prognosis impact of kinase activation on AML patients was only rarely evaluated. The most important studies related to FLT3 activating mutations, which implied an adverse outcome. Recent reports suggest that PI3 kinase (PI3K) activation may confer a poor survival to AML patients. Methods. Primary bone marrow blast cell samples from 92 patients registered for the LAM2001 trial of the GOELAMS were analyzed at diagnosis and PI3K constitutive activation was correlated with outcome. As previously reported (V Bardet, Haematologica, 2006, 91, 757-764), PI3K activation was established with the status of AKT phosphorylation on Ser 473, determined using either Western Blot analysis (in samples >90% blasts) or flow cytometry in the CD45Low positive population of blast cells, after 4 hours of cytokine and serum starvation. In such conditions, two groups of patients were defined, one with constitutive activation of PI3K (PI3K + ), contrary to the second (PI3K – ). Results. Median age at diagnosis was 46 (17,3-64,5) years. 42 patients were males and 50 were females. Leukocytosis was 12000/∝L (range 400-251800). Patients were classified in low, standard and high-risk cytogenetic subgroups in 16%, 61% and 23%, respectively. 17/79 (21,5%) had FLT3-ITD mutation, 9/60 (15%) had Ras (N-Ras or K-Ras) mutations and 18/72 (25%) had NPM mutations. 46 of 92 (50%) patients had constitutive PI3K activation (PI3K + group). In univariate analysis, no difference was observed between the two groups for all previously described parameters, except concerning FLT3 mutational status: 5/40 (12,5%) PI3K + patients had FLT3-ITD versus 12/39 (30%) in the PI3K- (p=0,048). All patients received one course of induction chemotherapy (3+7 regimen), and 31 (34%) a second induction course at day 15. Complete remission was obtained in 74 patients (80%) with no difference between the two groups (p=0,60). Among responders, 30 (41%) had autologous stem cell transplantation, 24 (32%) had allogenic bone marrow transplantation and 16 (22%) had consolidation chemotherapy. With a median follow-up of 26 months (range 3 days- 37 months), 48 patients died. Overall survival was 56% in the PI3K + group and 33% in the PI3K _ group (p=0.007). Among responders, 30 patients relapsed. Relapse free survival was 72% in the PI3K + group and
41% in the PI3K- group (p=0.001). In multivariate analysis, the PI3K activation plays a significant prognostic role on overall and relapse free survival, after adjustment for FLT3 status (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: drug-induced apoptotic response of
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 and 36: new cases of lead poisoning due to
Page 37 and 38: icance, from baseline to week 6 (p
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
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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
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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
Page 101 and 102:
Bortezomib 1.3 mg/m 2 days 1,4,8,11
Page 103 and 104:
Response was defined according to E
Page 105 and 106:
G-CSF can be used in neutropenic pa
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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
Page 123 and 124:
No major toxicity, neither hematolo
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enewal potential of X-RAR-positive
Page 127 and 128:
(50-99) respectively. Serial analys
Page 129 and 130:
cell-interaction, adhesion and acti
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0340 ALTERED FIBRIN CLOT STRUCTURE
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Conclusions. This study demonstrate
Page 135 and 136:
0354 FACTOR V LEIDEN HOMOZYGOUS GEN
Page 137 and 138:
Results. From July 2005 through Mar
Page 139 and 140:
0364 CLINICAL EFFICACY OF OXALIPLAT
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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
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Cytogenetics and molecular diagnost
Page 149 and 150:
0385 CYTOPLASMIC MUTATED NUCLEOPHOS
Page 151 and 152:
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
Page 157 and 158:
is 85%. Seven out of the 25 relapse
Page 159 and 160:
0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
Page 163 and 164:
successfully managed with GM-CSF di
Page 165 and 166:
49% for PCR positive patients (95%
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+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
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observed in all mice. Analysis of l
Page 175 and 176:
ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
Page 179 and 180:
One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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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
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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
Page 203 and 204:
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
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
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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
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inding lectin (MBL) gene by polymer
Page 239 and 240:
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
Page 247 and 248:
Myeloproliferative disorders - Clin
Page 249 and 250:
open-label, multi-centre study enro
Page 251 and 252:
iopsies after 6 and 12 months treat
Page 253 and 254:
Myeloproliferative disorders Chroni
Page 255 and 256:
ash, muscolar cramps, diarrhoea, he
Page 257 and 258:
induced significant apoptosis (mean
Page 259 and 260:
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
Page 265 and 266:
Myeloma and other monoclonal gammop
Page 267 and 268:
secutive patients with MM, referred
Page 269 and 270:
whether gene expression values may
Page 271 and 272:
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
Page 289 and 290:
0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
Page 295 and 296:
Results. A total of 396 patients we
Page 297 and 298:
C30 questionnaire, and the correspo
Page 299 and 300:
wave length of light of reflected r
Page 301 and 302:
0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
Page 305 and 306:
0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
Page 309 and 310:
p=0.014 and p=0.003, respectively).
Page 311 and 312:
0809 CURRENT APPROACH TO CHELATION
Page 313 and 314:
Thrombosis II 0814 UNSUSPECTED PULM
Page 315 and 316:
the 97.5th percentile (5.2 U/mL) ge
Page 317 and 318:
symptoms of DVT, 3 (7.89%) previous
Page 319 and 320:
Transfusion medicine and vascular b
Page 321 and 322:
tions (most bacterial, 2 malaria, 6
Page 323 and 324:
0844 INCREASED LEUKOCYTE-PLATELET I
Page 325 and 326:
0851 CORD BLOOD DERIVED MESENCHYMAL
Page 327 and 328:
SIMULTANEOUS SESSION II Chronic mye
Page 329 and 330:
0862 COMPARISON OF DASATINIB TO HIG
Page 331 and 332:
0867 COMPREHENSIVE GERIATRIC ASSESS
Page 333 and 334:
0872 MN1 INDUCES LEUKEMIA IN MICE A
Page 335 and 336:
0877 PAX5/TEL TRANSDUCED PRE-BI CEL
Page 337 and 338:
0882 CISPLATIN INDUCES THROMBIN GEN
Page 339 and 340:
have an early manifestation of typi
Page 341 and 342:
0892 INTEGRATION OF GENOME WIDE SNP
Page 343 and 344:
0897 THE PHENOTYPE OF JAK2V617F MUT
Page 345 and 346:
gest diverse sequences of NPM mutan
Page 347 and 348:
2004 to January, 2006. At enrollmen
Page 349 and 350:
with a p value of ≥ 0.10. Sets of
Page 351 and 352:
BRIC 126 and 4N1K) in cells lacking
Page 353 and 354:
sclerosis[NS] and 12 Mixed cellular
Page 355 and 356:
0927 MK-0457, A NOVEL MULTIKINASE I
Page 357 and 358:
Publication Only 0933 CLINICAL FEAT
Page 359 and 360:
HSCT from the available Asian as we
Page 361 and 362:
that the incidence of JAK2 mutation
Page 363 and 364:
without type 2 diabetes. Methods. T
Page 365 and 366:
pts (38.8%) that were isolated (abs
Page 367 and 368:
y using the Miltenyi CD34 isolation
Page 369 and 370:
0969 COMPARISON OF CD25 IMMUNOHISTO
Page 371 and 372:
cytes was 24 days (range 8-32 days)
Page 373 and 374:
a cytogenetic hallmark for M4/M5 su
Page 375 and 376:
normal human BM B progenitor cells
Page 377 and 378:
0994 INCIDENCE OF INVASIVE ASPERGIL
Page 379 and 380:
3 of disease relapse.TRM at day+100
Page 381 and 382:
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
Page 389 and 390:
ment details and thrombotic histori
Page 391 and 392:
1036 INCIDENCE AND SPECTRUM OF INFE
Page 393 and 394:
tinely by our stem cell lab prior t
Page 395 and 396:
tion to a translocation t(5;14)(q35
Page 397 and 398:
ment of CML and induces a high rate
Page 399 and 400:
due to reactivation and/or progress
Page 401 and 402:
1063 ABNORMAL METHYLATION STATUS OF
Page 403 and 404:
1069 CLINICAL RELEVANCE OF REGULATO
Page 405 and 406:
1076 SERUM LEVELS OF SOLUBLE HLA CL
Page 407 and 408:
patient is still undergoing intensi
Page 409 and 410:
nificant MVD differences were detec
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dictor of OS (p=0.004). High dose t
Page 413 and 414:
1099 ALTERATIONS IN THE NATURAL KIL
Page 415 and 416:
1105 CYTOGENETIC ABNORMALITIES IN 3
Page 417 and 418:
1110 CONSTITUTIVE ACTIVATION OF STA
Page 419 and 420:
efficacy results with a well-tolera
Page 421 and 422:
unmutated VH genes, and high and lo
Page 423 and 424:
Aims. Aim of this study was to pred
Page 425 and 426:
tested across a wide range of human
Page 427 and 428:
were incidentally diagnosed (52%).
Page 429 and 430:
ß2GP1 may be considered as determi
Page 431 and 432:
characterized in 198 β thalassaemi
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
Page 435 and 436:
to-pelvic or perineal trauma. No me
Page 437 and 438:
in age. High prevalence of LBM amon
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ecause some of the patients were or
Page 441 and 442:
of the drug is crucial to allow lon
Page 443 and 444:
egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
Page 447 and 448:
admitted to ICU were discharged des
Page 449 and 450:
events -Postoperative states: 9,19%
Page 451 and 452:
efficacy and decreased atherosclero
Page 453 and 454:
1217 INCIDENCE OF EARLY STAGE IDIOP
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1691GA and 1 homozygous 1691AA. The
Page 457 and 458:
1230 ASSOCIATION OF HEPARANASE GENE
Page 459 and 460:
posed, was: DF = (CD43%+FMC7%+CD79b
Page 461 and 462:
treatment of acute promyelocityc le
Page 463 and 464:
loaded group and 35 (70%) were non-
Page 465 and 466:
mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
Page 469 and 470:
ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
Page 475 and 476:
disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
Page 479 and 480:
phamide 750 mg/m 2 on day 1, vincri
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
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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
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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
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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
Page 531 and 532:
1466 ROS GENERATION AND APOPTOSIS I
Page 533 and 534:
1473 DIARRHEIC SYNDROME, A CLINICAL
Page 535 and 536:
gene fusion is an independent progn
Page 537 and 538:
1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
Page 541 and 542:
immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
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Hodgkin’s disease is well known,
Page 547 and 548:
gram provided a unique chance to de
Page 549 and 550:
even when ADP-induced plt activatio
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medullary involvement of multiple m
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
Page 559 and 560:
Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
Page 567 and 568:
El-Sharkawy, N., 0016 Elwahidi, G.,
Page 569 and 570:
Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
Page 573 and 574:
Jaksic, B., 0127, 0446 Jaksic, O.,
Page 575 and 576:
Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
Page 581 and 582:
Musto, P., 0254, 0401, 0422, 0569,
Page 583 and 584:
Papadavid, E., 1442 Papageorgiou, E
Page 585 and 586:
Probatova, N., 0704 Prochazka, V.,
Page 587 and 588:
Rykavicin, O., 0504 Ryningen, A., 0
Page 589 and 590:
Sirard, C., 0127, 0128 Sirigou, A.,
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Thiebaut, A., 0454 Thieblemont, C.,
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Vincenzi, C., 1060 Viniou, N.-A., 0
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Zouabi, H., 0503, 0999 Zoumbos, N.C
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12 th Congress of the European Hema
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12th Congress of the European Hematology ... - Haematologica

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