12th Congress of the European Hematology ... - Haematologica

More documents

Recommendations

Info

12 th Congress of the European Hematology Association sis. There were 30 pts with good, 70 pts with intermediate and 9 pts with unfavorable prognosis. Among 70 pts with interemediate risk cytogenetics, 67 pts had normal karyotype. The expression of P-gp in the whole group was from 0.2% to 84.3% (mean: 14.5% ±16.1). Pts with unfovorable prognosis had higher Pgp expression (24.4%, SD=21.3) than pts with interemediate (15.6%, SD=15.7), and pts with good risk cytogenetics (10.7%, SD=14.4). Using the Student’s t-test there was statistical significant difference in MDR1 expression between unfovorable and good risk group (p=0.033). The statistical analysis showed significant differences (p0.1% were associated with improved LFS and OS. AML patients with HGs in marrow sample in first CR have significant higher LFS (p
1110 CONSTITUTIVE ACTIVATION OF STAT1 AND STAT3 PROTEINS WITHOUT INTERFERON INDUCIBILITY: RELEVANCE TO THERAPY IN IGVH-UNMUTATED CLL PATIENTS J. Chumchalova, J. Navratilova, D. Klimesova, H. Francova, V. Kuhrova, Y. Brychtova, M. Doubek, D. Dvorakova, J. Mayer University Hospital Brno, BRNO, Czech Republic Background. STAT proteins play an important role in regulation of proliferation, differentiation, apoptosis, and immune response. STAT proteins are constitutively activated in hematopoetic cells, which are transformed by oncogenic tyrosine kinases and are also connected to pathology of variety leukemias and lymphomas. Tyrosine phosphorylation of STAT proteins allows formation of dimers, translocation to the nucleus and binding to specific DNA sequences within promoters of target genes, which leads to activation of transcription. Serine phosphorylation is not necessary to activate STATs, but it modulates gene activation induced by tyrosine phosphorylation. Constitutive phosphorylation of serine but not tyrosine in both STAT proteins was found in B-CLL cells. Aims. The aim of our study was to examine defects in STAT1 and STAT3 pathways in our CLL patients. Methods. We analyzed defects in STAT1 and STAT3 pathways after stimulation of cells with interferon γ (IFNγ) (10 ng/mL) and interferon α (IFNα) (5000 IU/mL). We evaluated 59 primary cultures derived from CLL patients with prevalency of B-CLL cells. Presence of STAT1 and STAT3 protein isoforms was detected by Western-blotting analysis using specific polyclonal and monoclonal antibodies. Results. Constitutive phosphorylation of serine and tyrosine residues of both STAT proteins was found in majority of CLL patients. STAT1 protein showed higher ratio of defect in phosphorylation of serine (69,6%) and tyrosine (43,5%) after induction by interferons compared to phosphorylation of serine (15,8%) and tyrosine (50%) of STAT3 protein. IFNα is more effective inductor of both phosphorylations in STAT1 and STAT3 proteins. Only tyrosine phosphorylation of STAT1 protein was markedly induced by IFNγ. Analysis of relationship STAT proteins and IgVHmutation status was performed. We did not found significant differences in phoshporylation of STAT1 and STAT3 proteins. IFNα induced only tyrosine phosphorylation of STAT1 protein in IgVH-unmutated patients compared to IgVH-mutated patients where the phosphorylation was induced by both IFNs. Analysis of IgVH-unmutated patients who required therapy showed higher proportion of constitutive phosphorylation without IFN inducibility in both STAT proteins compared to untreated patients. Consequently, the significant difference was found among IgVH-unmutated patients with or without therapy. Patients with therapy showed markedly higher proportion of constitutive phosphorylation without IFN inducibility of serine and tyrosine residues in STAT1 and serine residue in STAT3 proteins. On the contrary, these patients manifested a decrease of constitutive phosphorylation without IFN inducibility on tyrosine residue in STAT3 protein. Conclusions. Our results show that majority of CLL patients have constitutive phosphorylation of both STAT proteins. IFNα was shown to be a more effective inductor in comparison with IFNγ. Presence of constitutive phosphorylation without IFN inducibility of STAT1 and STAT3 proteins is increased in IgVH-unmutated CLL patients who required therapy. Supported by grant NR8443-3/2005 provided by IGA MZCR 1111 CD28 AND ICOS GENE POLYMORPHISMS ARE ASSOCIATED WITH BCELL CHRONIC LYMPHOCYTIC LEUKEMIA (B-CLL) I. Frydecka, 1 K. Suwalska, 2 A. Tomkiewicz, 2 E. Pawlak, 2 L. Karabon, 2 T. Dobosz, 1 A. Jonkisz, 1 A. Lebioda, 1 K. Kapelko-Slowik, 1 K. Kuliczkowski, 1 D. Wolowiec1 1 2 Medical University, WROCLAW, Poland; Institute of Immunology and Experimental, WROCLAW, Poland Background. There are strong evidences that altered immunological function entails an increased risk of B- CLL. T cell-specific surface receptors CD28 and inducible co-stimulator (ICOS) are main costimulatory molecules expressed on cell surfaces and provide regulatory signals for T-cell activation. CD28 potently enhances T-cell functions essential for effective antigen-specific immune responses. Unlike the constitutively expressed CD28, ICOS is induced on the T-cell surface and does not upregulate the production of IL-2, but induces the synthesis of IL-4. Aim. The extended study was undertaken to evaluate the association between the T17int3C CD28 gene polymorphism, microsatelite (GT)n polymorphism in intron 4 of the ICOS gene and susceptibility to B-CLL in a Polish population. Methods. One hundred twenty four B-CLL patients and 202 healthy subjects were studied. Allele identification was achieved by 12 th Congress of the European Hematology Association PCR amplification. The amplified product for SNP (single-nucleotide polymorphism) loci was purified and minisequenced using the commercial kit SnapShot of PE Applied Biosystems. The dinucleotide repeat polymorphism was studied by PCR and fuorescence based technique. The products were analyzed on the ABI PRISM 310 Genetic Analyzer (ABI PRISM 310 capilary elctrophoresis system). Results. The distribution of the CD28IVS3+17C/T alleles and genotypes presented significant differences in B-CLL patients and healthy controls. The presence of CD28IVS3 + 17C allele and CD28IVS3+17(C/C+C/T) genotype increased the odds of B-CLL by 1.97 and 2.07 [p=0.0019, 1.2755~95%CI ~3.0313 and p=0.0033, 1.2686~95%CI ~3.3778, respectively]. Global distribution of ICOS alleles was significantly different in B-CLL patients and healthy controls (p= 0.000005). The results showed that (GT)9 allele increased risk of B-CLL 2,3 times [p=0.0294, OR =2.345, 1.0700~95%CI~5.1419] while frequency of the (GT)12 was significantly decreased in patients [p=0.0002, OR =0.4307, 0.4307]. Moreover, distribution of genotypes differed between patients and healthy controls (p=0.0076). The GT9/GT11 genotype was overexpressed in B-CLL patients compared with control subjects (p=0.03, OR= 2.3457, 1.0700~95%CI ~5.1419), while genotypes GT12/GT12, was more frequent in control subjects [p=0.0024, OR=0.0831, 0.0195~95%CI ~0.6306] Summary. Our results suggest that the CD28 T17int3C gene polymorphism and microsatelite ICOS gene (GT)n polymorphism contribute to genetic susceptibility to B-CLL 1112 TRYPTASE AS NOVEL TUMORMARKER IN CLINICAL HEMATOLOGY: EVALUATION OF 1041 PATIENTS W.R. Sperr, 1 A. El-Samahi, 1 M. Girschikofsky, 2 S. Winkler, 1 H. Semper, 1 H. Agis, 1 C. Sillaber, 1 G. Endler, 1 H. Rumpold, 1 D. Lutz, 2 P. Valent1 1 2 Medical University of Vienna, VIENNA; KH der Elisabethinen, Dept of Int Med I, LINZ, Austria Background. Tryptase is a term used for a family of trypsin-like serine proteases primarily produced and stored in mast cells. Recent data suggest, that tryptase is expressed in neoplastic cells in various myeloid neoplasms. The aim of the present study was to determine whether tryptase may serve as a marker of disease in patients with hematologic neoplasms. Aims. The aim of this study was to determine the diagnostic and prognostic significance of tryptase in patients (pts) with hematologic neoplasms. Methodes. Tryptase levels were determined in 906 pts with hematologic malignancies, including myeloproliferative disorders (MPD, n=153), myelodysplastic syndromes (MDS, n=233), acute myeloid leukaemia (AML, n=317), and systemic mastocytosis (SM, n=71), and in 137 pts with reactive leukocytosis/thrombocytosis or idiopathic cytopenia, by fluoroenzyme-immunoassay. Moreover, tryptase was analyzed in 165 healthy subjects, 80 pts with non hematologic disorders. Results. For this purpose, serum tryptase levels were determined in 906 patients (pts) with hematologic malignancies, including myeloproliferative disorders (MPD, n=153), myelodysplastic syndromes (MDS, n=233), acute myeloid leukaemia (AML, n=317), and systemic mastocytosis (SM, n=71), and in 137 pts with reactive leukocytosis/thrombocytosis or idiopathic cytopenia, by fluoroenzyme-immunoassay. Moreover, tryptase was analyzed in 165 healthy subjects, 80 pts with non hematologic disorders. In 90% of healthy controls serum tryptase levels ranged between 2.4 ng/mL and 9.5 ng/mL (median: 5.7 ng/mL; range in all pts: >0.1-18 ng/mL). Among pts with non hematologic disorders, slightly elevated serum tryptase levels (up to 24 ng/mL) were detectable in 6/18 pts with severe renal failure and in 3/29 pts with helminth infections. In the majority of pts with reactive leukocytosis/thrombocytosis or idiopathic cytopenia serum tryptase was within the normal range (″15 ng/mL), as were most pts with lymphoid neoplasms. Among myeloid neoplasms, elevated tryptase levels were recorded in 83% of the pts with SM, 37% of pts with AML, 34% of the pts with CML, and 24% of the pts with MDS. The highest tryptase levels were found in pts with SM or AML-M4eo. In pts with CML treated with imatinib, elevated tryptase levels were found to be associated with an unfavourable prognosis concerning survival (tryptase ″15 ng/mL: 100%; tryptase >15 ng/mL: 71%, after 60 months, 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 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
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
Page 93 and 94:
PCH97-19) were studied. Conventiona
Page 95 and 96:
of erythroid colonies was reduced i
Page 97 and 98:
0245 POTENT AND SELECTIVE INHIBITIO
Page 99 and 100:
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
Page 107 and 108:
ence and functional activity of CD8
Page 109 and 110:
itating tumor development, or engag
Page 111 and 112:
phoma and SNT-13, -15 were establis
Page 113 and 114:
usage (2/20 ie 10%) were observed.
Page 115 and 116:
0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
Page 117 and 118:
(range, 1-6) and 11 treatment cycle
Page 119 and 120:
0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
Page 121 and 122:
functional activity was confirmed b
Page 123 and 124:
No major toxicity, neither hematolo
Page 125 and 126:
enewal potential of X-RAR-positive
Page 127 and 128:
(50-99) respectively. Serial analys
Page 129 and 130:
cell-interaction, adhesion and acti
Page 131 and 132:
0340 ALTERED FIBRIN CLOT STRUCTURE
Page 133 and 134:
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
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 and 192:
previously reported, a single cours
Page 193 and 194:
0497 SINGLE AGENT CLORETAZINE (VNP4
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
Page 243 and 244:
formation (in total 28 samples). Ti
Page 245 and 246:
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
Page 261 and 262:
the therapy of choice for POEMS is
Page 263 and 264:
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
Page 273 and 274:
0710 CLINICO-PATHOLOGICAL FEATURES,
Page 275 and 276:
patients presented a stage IV disea
Page 277 and 278:
plete remission or recurrent diseas
Page 279 and 280:
known at NHL diagnosis, were includ
Page 281 and 282:
0731 THE IMPACT OF HIV ON NON-HODGK
Page 283 and 284:
patients had died of their underlyi
Page 285 and 286:
scripts and proteins most affected
Page 287 and 288:
modulated after 24 h (37 up- and 59
Page 289 and 290:
0753 A SUSTAINED REMISSION OF IDIOP
Page 291 and 292:
and treatment, has rarely been syst
Page 293 and 294:
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
Page 303 and 304:
erozygous mother has a more severe
Page 305 and 306:
0794 CARDIAC MANIFESTATIONS IN A BR
Page 307 and 308:
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
Page 411 and 412: dictor of OS (p=0.004). High dose t
Page 413 and 414: 1099 ALTERATIONS IN THE NATURAL KIL
Page 415: 1105 CYTOGENETIC ABNORMALITIES IN 3
Page 419 and 420: efficacy results with a well-tolera
Page 421 and 422: unmutated VH genes, and high and lo
Page 423 and 424: Aims. Aim of this study was to pred
Page 425 and 426: tested across a wide range of human
Page 427 and 428: were incidentally diagnosed (52%).
Page 429 and 430: ß2GP1 may be considered as determi
Page 431 and 432: characterized in 198 β thalassaemi
Page 433 and 434: 1155 PLATELET AGGREGATION IN CHILDR
Page 435 and 436: to-pelvic or perineal trauma. No me
Page 437 and 438: in age. High prevalence of LBM amon
Page 439 and 440: ecause some of the patients were or
Page 441 and 442: of the drug is crucial to allow lon
Page 443 and 444: egarding cost analysis of ASCT in G
Page 445 and 446: ID Allo-BMT, 1 family one mismatche
Page 447 and 448: admitted to ICU were discharged des
Page 449 and 450: events -Postoperative states: 9,19%
Page 451 and 452: efficacy and decreased atherosclero
Page 453 and 454: 1217 INCIDENCE OF EARLY STAGE IDIOP
Page 455 and 456: 1691GA and 1 homozygous 1691AA. The
Page 457 and 458: 1230 ASSOCIATION OF HEPARANASE GENE
Page 459 and 460: posed, was: DF = (CD43%+FMC7%+CD79b
Page 461 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:
show all

12th Congress of the European Hematology ... - Haematologica

Create successful ePaper yourself

Delete template?

Save as template?