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12 th Congress of the European Hematology Association healthy controls at National Taiwan University Hospital (Taipei, Taiwan). All the molecules were quantified using ELISA. Concentrations in the AML patient and healthy control groups were compared using Student’s t test. The receiver operating characteristic (ROC) curve was constructed, and the area under the ROC curve (AUROC) was calculated. Survival status was investigated by using the Kaplan-Meier survival curve and log-rank test. Multivariate Cox regression analyses were also used to estimate prognosis. Results. The OPN level was significantly higher (p
0487 MUTATIONAL STATUS OF NUCLEOPHOSMIN (NPM1) AND FLT-3 GENES ARE STRONG PREDICTORS OF THE OUTCOME IN PATIENTS WITH CYTOGENETIC INTERMEDIATE-RISK ACUTE MYELOID LEUKEMIA UNDERGOING AUTOLOGOUS STEM-CELL TRANSPLANTATION M. Torrebadell, 1 M. Camós, 2 S. Brunet, 3 M. Rozman, 2 M. Pratcorona, 2 J. Nomdedeu, 3 A. Carrio, 2 D. Costa, 2 D. Colomer, 2 E. Carreras, 2 E. Campo, 2 J. Sierra, 3 E. Montserrat, 2 J. Esteve 2 1 Hospital Clinic, BARCELONA; 2 Hospital Clínic, BARCELONA; 3Hospital de Sant Pau, BARCELONA, Spain The modality of post-remission therapy in AML is mainly based on cytogenetics. However, there are several cytogenetic categories, such as the intermediate-risk subgroup, that include patients with a highly heterogeneous prognosis. In this subset of patients, molecular markers such as mutations of NPM1 and flt-3 genes might be useful to determine prognosis more precisely. We analyzed the predictive value of these molecular markers in patients with AML receiving autologous stem-cell transplantation (autoSCT). Thirty-seven patients (age: 53, 15-66; 51% female) diagnosed with AML of intermediate-risk cytogenetics (normal karyotype, n=23) and submitted to autoSCT in first complete remission (CR1) during 1995-2006 were included in the analysis. Pre-transplant therapy was similar in all patients, consisting of one (n=32) or two cycles (n=5) of standard induction chemotherapy (ICE, n=8, IDICE, n=29) and one cycle of high-dose ara-C-based consolidation chemotherapy, according to three sequential trials (CETLAM protocols LMA-94, LMA-99, and LMA-2003). Conditioning regimen contained TBI in most cases (86%) and the stem-cell source was peripheral blood in all patients. Internal tandem duplication of flt-3 (flt-3 ITD) and exon 12 NPM1 mutations were studied in diagnostic samples by either PCR or RT-PCR following standard methods and visualized by means of Genescan analysis. After a median follow-up of 66 months (6-122), 12 patients relapsed after autoSCT, this resulting in a 5-year OS and LFS of 56±9% and 50±9%, respectively. According to molecularly-defined risk, three different subgroups of patients were considered: group 1 (NPMmut: n=12, 32%), constituted by patients with mutated NPM1 without flt-3 ITD; group 2 (NPM-neg: n=20, 54%), which included patients without NPM1 or flt- 3 ITD; and group 3 (flt-3 ITD: n=5, 13%), defined by flt-3 ITD regardless NPM1 mutational status. The only variables with prognostic value for survival after autoSCT were flt-3 ITD, which conferred an adverse prognosis (5-yr OS: 62%±10% vs. 20%±18%, p=0.028), and molecular NPM1/flt3 category (5-yr OS: 90%±10% [group 1] vs. 48%±13% [group 2] vs. 20%±18% [group 3], p=0.02; see Figure 1). In conclusion, autoSCT is an effective post-remission strategy in patients with NPM1-mutated AML, whereas flt-3 ITD identifies a high-risk population who does not benefit from this procedure. For the subgroup of patients lacking NPM1 and flt-3 mutations, search of other molecular markers adding prognostic information is warranted in order to assess the role of different postremission options. Figure 1. 12 th Congress of the European Hematology Association 0488 ANALYSIS OF THE ASSOCIATION OF ICAM-1 AND PECAM-1 POLYMORPHISMS AND THE DEVELOPMENT OF DIFFERENTIATION SYNDROME IN ACUTE PROMYELOCYTIC LEUKEMIA A.I.D. Dore, 1 B.A.A. Santana-Lemos, 1 L.F.F. Dalmazzo, 1 V.M. Coser, 2 F.L.S. Santos, 1 A.S.G. Lima, 1 R.H. Jacomo, 1 L.L. Figueiredo-Pontes, 1 J. Elias Junior, 1 R.P. Falcao, 1 W.V. Pereira, 2 E.M. Rego1 1 2 University of Sao Paulo, RIBEIRÃO PRETO; University os Santa Maria, SANTA MARIA, Brazil The use of all trans-retinoic acid (ATRA) is the base of treatment of Acute Promyelocytic Leukemia (APL) and constitutes the paradigm of differentiation therapy. In general, ATRA is well tolerated, but may be associated with a potentially lethal side effect, referred to as Retinoic Acid or Differentiation Syndrome (DS), which is characterized by fever, pleural and pericardial effusions, respiratory distress, weight gain and pulmonary infiltrates on chest radiography. The cellular and molecular mechanisms of DS are poorly understood, and involve changes in the adhesive qualities and cytokine secretion of leukemic cells during ATRAinduced differentiation. Since leukocyte extravasation is a key event in DS pathogenesis, we analyzed the association between the polymorphisms at exon 6 of ICAM-1 (K469E) and exon 3 of PECAM-1 (L125V) genes and DS development in APL patients treated with ATRA and anthracyclines. Bone marrow (BM) or peripheral blood (PB) specimens from 127 patients with APL were collected at diagnosis. PB samples from 248 healthy volunteers were used as controls. The genetic confirmation of the PML/RARα rearrangement was done by RT-PCR using the BIO- MED-1 protocol. DS was diagnosed in 23/127 (18.1%) APL patients, at an average of 11.5 days after the start of ATRA (between the 4 th and 20 th days). We did not demonstrate any difference between the group of leukemic patients with and without DS regarding age, gender, white blood cells counts, hemoglobin value or platelets counts. All patients who developed DS presented respiratory distress associated with increased ground-glass opacity in chest radiographies and, other accompanying symptoms were: fever not attributable to infection (65.2%), generalized edema (37.5%), weight gain (37.5%) and impairment of renal function (8.6%). The genotype frequencies of ICAM-1 were GG 33.0%, GA 50.8% and AA 16.2% in APL patients and GG 8.0%, GA 54.6% and AA 37.4% in control group. For PECAM-1, these frequencies were CC 10.2%, CG 60.2% and GG 29.2% in APL patients and CC 22.3%, CG 57.0% and GG 20.7% in control group. These genotype frequencies of both groups did not deviate significantly from the predicted frequency using Hardy-Weinberg equilibrium. APL patients presenting the AA genotype at exon 6 of ICAM-1 had a significantly increased risk of developing DS with a relative risk of 2.6 (95% confidence interval: 1.2-5.6). The AA genotype frequency in APL patients with and without DS was, respectively, 33% and 12.6% (p=0.04). On the other hand, no significant association was detected between L125V polymorphism at exon 3 of PECAM-1 and DS development. Our results suggest that susceptibility to DS in APL patients may be influenced by genetic variation in adhesion molecules loci. 0489 PHARMACOKINETIC/PHARMACODYNAMIC CORRELATION WITH CLINICAL RESPONSES IN A PHASE 1 STUDY OF PATIENTS WITH RELAPSED/REFRACTORY ACUTE LEUKEMIAS TREATED WITH SNS 595 M.R. Arkin, 1 R. Ricklis, 2 J. Lancet, 3 F. Giles, 4 U. Hoch, 1 D. Stockett, 1 Y Zhu, 1 G. Michelson, 1 J.A. Fox, 1 J.E. Karp2 1 Sunesis Pharmaceuticals, SOUTH SAN FRANCISCO; 2 Sidney Kimmel Comprehensive Cancer Cente, BALTIMORE; 3 H. Lee Moffitt Cancer Center and Researc, TAMPA; 4MD Anderson Cancer Center, HOUSTON, USA Background. SNS-595, a novel cell-cycle active compound that disrupts DNA replication forks and triggers DNA damage responses, G2 arrest, and apoptosis, is in phase 1 and 2 clinical trials in hematologic and solid malignancies. Preliminary clinical, pharmacokinetic (PK) and correlative results from an on-going escalating-dose phase 1 trial of SNS- 595 in refractory acute leukemias are presented. Aims. Objectives: 1) establish safety, tolerability and MTD of SNS-595 given on 2 schedules; 2) characterize PK; 3) assess clinical activity; 4) explore potential biomarkers of mechanism-based activity and patient stratification. Methods. SNS-595 IV dosing: Arm A: days 1, 8 and 15; Arm B: days 1, 4, 8 and 11; minimum cycle lengths were 42 days and 39 days, respectively. Starting doses were18 mg/m 2 (Arm A) and 9 mg/m 2 (Arm B), with escalation by cohort. PK samples and pretreatment blood and bone marrow aspirates were collected from all patients for exploratory analyses haematologica/the hematology journal | 2007; 92(s1) | 181
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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
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: expression along with a decreased C
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
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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
Page 305 and 306:
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
Page 351 and 352:
BRIC 126 and 4N1K) in cells lacking
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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
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HSCT from the available Asian as we
Page 361 and 362:
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
Page 369 and 370:
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
Page 377 and 378:
0994 INCIDENCE OF INVASIVE ASPERGIL
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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
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
Page 395 and 396:
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
Page 401 and 402:
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
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
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:
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