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12 th Congress of the European Hematology Association 0657 ASSESSING THE LONGTERM EFFECT OF IMATINIB MESYLATE IN BONE METABOLISM OF PATIENTS WITH CHRONIC MYELOID LEUKEMIA C. Kartsios, M. Christopoulou, A. Lazaridou, E. Verrou, M. Koltsida, A. Banti, C. Chatziangelidou, E. Katodritou, K. Zervas Theagenion Cancer Hospital, THESSALONIKI, Greece Background and Aims. Imatinib mesylate (IM) inhibits several tyrosine kinases, including BCR-ABL, the C-KIT receptor, and the platelet-derived growth factor receptors α and β, all of which are associated with disease. Recently, IM has been shown to alter bone metabolism by inhibiting osteoclast differentiation and function in in vitro models. In the present study, bone metabolism markers were determined in a cohort of chronic myeloid leukaemia (CML) patients who were extensively treated with IM. Patients and Methods. Seventeen CML patients [M/F: 11/6, median age: 62(48-74) years, median time on IM: 48(10-56) months, median daily dose of IM: 400(400-800) mg] and 10 healthy volunteers [M/F: 7/3, median age: 57(38-64) years] were studied. All CML patients were in chronic phase when IM was started. At the time of study, 13/17 patients were in complete cytogenetic response (cR), one patient was in partial cR and 3 patients were in hematological remission. We measured the plasma levels of intact parathyroid hormone (PTH) and the serum levels of total calcium (Ca) and phosphate (P). Evaluation of the bone formation was made by measuring total alkaline phosphatase (ALP), procollagen type I N-terminal propeptide (PINP) and osteocalcin (OSC). Bone resorption was assessed by determination of the plasma C-telopeptide of collagen cross-links (CTX). None of the patients had metabolic bone disease, and none was receiving medications known to influence the metabolism of calcium. Results. Hypocalcemia (total Ca 5% of patients are reported in the table. Grade 3/4 hematologic AEs for dasatinib were 2-3 times greater compared to those for nilotinib. Biochemistry abnormalities occurring in > 5% of nilotinib patients included lipase increase in 16.8%, elevated bilirubin in 10.3%, and hypophosphatemia in 9.7%; dasatinib patients experienced hypophosphatemia in 13% and hypocalcemia in 246 | haematologica/the hematology journal | 2007; 92(s1) 9%. Grade 3/4 non-hematologic AEs such as pleural/pericardial effusions were also higher for dasatinib than nilotinib. Summary and conclusions. The toxicity profiles of the second generation TKIs for imatinib resistant/intolerant CML-AP are different. Nilotinib’s lower rates of Grade 3/4 hematologic AEs and GI hemorrhage may result in reduced resource utilization. Further research is warranted to assess the economic impact of the differences in safety profiles. Table 1. Grade 3/4 AE rates: nilotinib v. dasatinib. 0659 IMATINIB EFFICACY AND TOLERABILITY IN ADVANCED AGE (>70 YEARS) CML PATIENTS V. Giai, 1 D. Ferrero, 2 M. Genuardi, 2 M. Strugli, 2 P. Pregno, 3 G. Rege-Cambrin, 4 A. Darbesio, 5 C. Boccomini, 6 M. Pini, 7 M. Boccadoro1 1 Azienda Ospedaliera San Giovanni Battist, TORINO; 2 Div. di Ematologia Universitaria, TORINO; 3 Azienda Ospedaliera S. Giovanni Battista, TORI- NO; 4 Azienda Ospedaliera San Luigi Gonzaga, ORBASSANO, TORINO; 5 Azienda Ospedaliera di Chivasso, CHIVASSO, TORINO; 6 Azienda Ospedaliera Cardinal Massaia, ASTI; 7 Azienda Ospedaliera SS Antonio e Biagio, ALESSANDRIA, Italy In the last years, CML prognosis had improved after introduction of tyrosine-kinase inhibitor imatinib-mesylate, that induces a complete cytogenetic response in about 80% of patients when used as a front-line therapy in chronic phase (O'Brien SG et al. N Engl J Med. 2003;348: 994- 1004) However, the optimal CML treatment in advanced age has not been definitely established. Before imatinib advent, old CML patients were handled just with palliative chemotherapy because of the impossibility for such patients to tolerate bone marrow transplantation or α interferon. Moreover, age is a prognostic negative factor for survival in CML (Sokal JE et al.: Blood 1984; 63: 789-99); therefore, most of old CML patients likely died of blastic phase CML. Imatinib has opened new therapy opportunities for advanced age patients. However, in spite of a median age for CML patients around 60, most of Imatinib studies mainly involved patients below that age. Two papers actually reported similar tolerance and efficacy of imatinib below and above the age of 60 (Cortes J et al.: Cancer. 2003; 98:1105-13; Latagliata R et al.: Leuk Res. 2005; 29:287-91) but no information has been provided about older patients, above the age of 70. Indeed, median age was 66 in one of the two papers and not reported in the other. Therefore, some doubts still exist about imatinib tolerability and cost effectiveness in old patients. In this study, we evaluate Imatinib tolerance and efficacy in 37 CML patients at or above the age of 70 (median age at the beginning of imatinib treatment was 76, range 70-87). One patient was treated in blastic phase, four in accelerated, one in second chronic and 31 in first chronic phase. Sokal score of first chronic phase patients was: low risk in 6 patients, intermediate in 18 and and high risk in 6. Seventeen chronic phase patients received imatinib as a front-line treatment, the other had received different previous therapies. The great majority presented with associated comorbidities. Grade 3-4 fluid retention was significantly more frequent (13%) than previously reported for younger patients. Conversely, the frequency of other hematological (neutropenia and thrombocytopenia) and extra-hematological toxic effects (cutaneous
ash, muscolar cramps, diarrhoea, hepatotoxicity), was not different from that reported in literature. Only 5 of 37 patients with severe comorbidities discontinued imatinib therapy for toxicity. Response rate (87% complete hematological and 56% complete cytogenetical remission in chronic phase patients) was just a little lower than reported for younger patients. All patients treated in 1st chronic phase are alive after a median 4 year follow up. Five of the 6 patients treated in advanced phase died (4 of CML progression, 1 of second neoplasm) at 3-25 months from diagnosis. In conclusion, this study shows that Imatinib therapy can be fairly tolerated and provide cytogenetic complete responses and long-term survival also in advanced age patients in chronic phase CML. It can be regarded as the treatment of choice for very old patients too, unless affected by severe comorbidities with short life expectancy. 0660 HYPOPHOSPHATAEMIA IN PATIENTS RECEIVING IMATINIB THERAPY A.-M. Watson, L. Dunlop, J. Gallo, M. Harvey, D. Heaton, P. Motum, D. Rosenfeld Liverpool Hospital, LIVERPOOL BC, Australia Background. A recent report found a high incidence of hypophosphataemia and changes in bone metabolism in patients receiving imatinib therapy. 1 Aims. To determine whether there is a similar significant incidence of hypophosphataemia in patients receiving long-term imatinib therapy for haematological disorders within our institution and identify any factors that may be linked to development of hypophosphataemia. Methods. The records and biochemistry results of patients receiving imatinib therapy for haematological disorders for >1 month duration were reviewed to identify development of hypophosphataemia (phosphate
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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
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one marrow and peripheral blood ste
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ecently suggested (Boissel et al.,
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0378 SAFETY AND EFFICACY OF THE TER
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Cytogenetics and molecular diagnost
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0385 CYTOPLASMIC MUTATED NUCLEOPHOS
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0390 ELTROMBOPAG RAISES PLATELET CO
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factor for the achievement of CR wa
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The cases of RAS showed two peaks o
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is 85%. Seven out of the 25 relapse
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0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
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successfully managed with GM-CSF di
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49% for PCR positive patients (95%
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+8 (1 PR+1 HI) and 14/24 pts with c
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(e.g. bcr-abl leading to CML). CSC
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0438 TERC MUTATIONS ANALYSIS IN PAT
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observed in all mice. Analysis of l
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ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
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One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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genesis of acute myeloid leukaemia
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polymorphism at nucleotide 4889 of
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expression along with a decreased C
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0487 MUTATIONAL STATUS OF NUCLEOPHO
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previously reported, a single cours
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0497 SINGLE AGENT CLORETAZINE (VNP4
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ly received melphalan-based chemoth
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were similar among the 3 groups. Ho
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Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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: Myeloproliferative disorders Chroni
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
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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
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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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
Page 387 and 388:
1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
Page 401 and 402:
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
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
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efficacy results with a well-tolera
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unmutated VH genes, and high and lo
Page 423 and 424:
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
Page 431 and 432:
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
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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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