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12 th Congress of the European Hematology Association time was 50 minutes, and median hospitalization duration was 2 1/2 days. Postoperative complications were minimal and included acute chest syndrome in 4 SCA patients after cholecystectomy. No fatalities or other postoperative complications were noted. Bivariate analysis showed that patients with regular blood transfusions and joint necrosis were more likely to undergo splenectomy and/or cholecystectomy (p
Thrombosis II 0814 UNSUSPECTED PULMONARY EMBOLISM: IMPACT ON CANCER PATIENTS' SURVIVAL P. Rodriguez Otero, R. Lecumberri, R. García Muñoz, E. Ruiz de Gaona, E. Rocha, J.A. Páramo University clinic of Navarra, PAMPLONA, Spain Background. The association between cancer and thrombosis is well established. The development of a thrombotic episode, either deep venous thrombosis (DVT) or pulmonary embolism (PE), significantly relates with worse cancer prognosis and shorter survival. With the use of multidetector computed tomography (MDCT) for the staging and follow-up of cancer patients, the diagnosis of incidental PE is increasing, but its clinical relevance in cancer patients is yet unknown. Aims. To describe the clinical features and outcomes of adult cancer patients diagnosed with unsuspected PE using MDCT, comparing completely asymptomatic patients and patients with non-specific symptoms subsequently attributed to PE. Methods. Retrospective analysis of consecutive cancer patients diagnosed with unsuspected PE by MDCT performed for disease staging or follow-up. Clinical data and D-dimer levels were assessed at diagnosis. Statistical analysis was performed using Chisquare tests with SPSS v11.0 software. Results. Between February 2002 and September 2006, 63 cancer patients (mean age 58±12 years, 47.6% males and 52.4% females) were diagnosed with incidental PE. The most frequent histologic type of cancer was adenocarcinoma (58.7%), especially gastro-intestinal. Most patients (66.7%) had metastatic disease at the time of the PE diagnosis. 58.7% of unsuspected PE were found at main pulmonary arteries, 27% at lobar arteries, while 14.3% were at segmental or subsegmental level. Clinical records showed that 58.7% of patients presented clinical symptoms that could be attributed to PE. During follow-up (median 17 months), 27 patients (42.9%) died, most of them due to cancer progression. Mortality was significantly lower in completely asymptomatic patients than in patients with non-specific symptoms subsequently attributed to PE (29% vs 57%; p=0.032). In adition, mortality was related to higher D-dimer levels at diagnosis (607 ng/mL vs 474 ng/mL; p=0.048). No significant association between mortality and age, sex, cancer stage or subtype or PE location was found. Conclusions. The absence of clinical symptoms of PE in cancer patients with unsuspected PE diagnosed by MDCT seems to be associated with a better prognosis of the neoplastic disease than patients with symptoms later attributed to PE. pecial attention to signs and symptoms suggestive of PE in this population is required, in order to achieve an early diagnosis and treatment. D-Dimer levels could be prospectively evaluated as prognostic markers after diagnosis of unsuspected PE. 0815 COINHERITANCE OF FV-LEIDEN MUTATION AND FV-HR2 P. Makris, M.P. Makris, S.I. Papamichos, A. Kanidis, P.E. Makris Aristotle University of Thessaloniki, THESSALONIKI, Greece The activated protein C resistance (APCr) phenotype is found approximately in 40% of thrombophilic patients. The factor V gene Leiden (Arg506Gln) mutation is considered interesting, looking for other factor V gene mutations associated to thrombophilia: The HR2 haplotype, the factor V Cambridge (Arg306Thr), the factor V Hong Kong (Arg306Gly) and the FV Liverpool (Ile359Thr). Because both factor V R506Q and the HR2 haplotype are very frequent, the effect of their coinheritance on the risk of venous thromboembolism may present a clinically relevant issue, and screening for HR2 in carriers of factor V R506Q should be considered. For this purpose we studied the presence of mutations in a group of 90 symptomatic patients (who suffered from one or more thromboembolic events). DNA was extracted from whole blood using the Qiagen extraction kit and polymorphism was determined by PCR method. Using the CVD strip assay, we found out that 22 patients were carriers of the FV Leiden mutation, 7 of the HR2, 10 of the G20210A polymorphism of prothrombin, 19 of the L34 mutation of XIII, 8 of the b-Fib 455G>A of fibrogen and 12 were homozygote (4G/4G) of PAI-1. Among these patients, a young individual was found to be double heterozygote, carrying FV Leiden and FV HR2. This, 21 year-old patient, suffered an episode of pulmonary embolism. A gene mutation test took place, because his mother in the age of 47 presented a thrombosis of the left hand and she was found to be heterozygote for the FV Leiden mutation. His grandmother passed away in the age of 68 because of ischemic stroke. Haemostasis control was normal, except from the pathological value of aPCR (39 sec, normal values >120 sec). The patient was prescript antivitamin-k for a long-term treatment. Double heterozygosity for factor V R506Q and HR2 conferred a 3- to 4-fold increase in the relative risk of venous thromboembolism compared with factor V R506Q alone. No increase in risk of venous thromboembolism could be demonstrated when the HR2 haplotype was associated with inherited thrombophilic defects other than factor V R506Q. The median age at first event was lower when the 2 defects were associated (46 v 52 years). 0816 RISK FACTORS AND SEQUELAE OF CEREBRAL VEIN THROMBOSIS: A FIVE YEAR RETROSPECTIVE AUDIT D. Costello, 1 M. Tharmabala, 2 F. Ni Ainle, 2 M. Spooner, 2 N. Appleby, 2 P. Murphy2 1 2 Beaumont Hospital, DUBLIN; Haematology Dept. Beaumont Hospital, DUBLIN, Ireland Background. Cerebral vein thrombosis (CVT) is a rare cause of neurological dysfunction that has, in recent years been diagnosed more frequently, in part due to improved non-invasive diagnostic techniques. A recent meta-analysis that re-evaluated the true natural history of CVT has identified a lower mortality rate and long-term prognosis than previously reported. The annual incidence is approximately 3-4 cases per million 1 however it can be associated with significant morbidity. A prothrombotic risk factor or direct cause is found in 85% of patients. The risk of sinus thrombosis is increased in the last trimester of pregnancy and after delivery 2 and the frequency of peripartum and postpartum sinus thrombosis is 12 cases per 100,000. 3 A study by Cantu et al. concluded that CVT during pregnancy and puerperium, while of more acute onset with a progressive course is often benign 2 Little data exists on the incidence of recurrent sinus thrombosis in women who have had a first event. In one series of 68 cases, no recurrent events occurred. 5 A systematic review by Dentali et al. showed the incidence of recurrence to be 2.8% in a combined cohort of almost 1100 patients. Almost ninety percent of surviving patients either recover fully or have only a mild functional or cognitive deficit. 6 Objectives. In the light of this recent metaanalysis, we evaluated risk factors, morbidity and mortality associated with CVT in a single Irish centre. Patient and methods. A retrospective audit was performed of patients diagnosed with CVT in an Irish hospital during January 2001 to July 2006, evaluating presenting symptoms, risk factors, survival and neurological sequelae. Results. Eighteen patients were identified, with a median age of 31 years. The commonest presenting symptoms were headache, vomiting and visual disturbance. 77% had at least one risk factor. 39% of events were associated with oral contraceptive use, pregnancy or postpartum state. 11% were associated with a local infection. 6% experienced a recurrent CVT. 6% died as a direct result of the event. 23% developed permanent neurologic deficit. Conclusions. Our study identified similar risk factors and rates of morbidity and mortality to those in recent literature, demonstrating that CVT has a more benign natural history than previously suspected. References 12 th Congress of the European Hematology Association 1. Stam, Jan. Thrombosis of the cerebral veins and sinuses. NEJM 2005;352:1791-8 2. Cantu C, Barinagarrementaria F. Cerebral vein thrombosis associated with pregnancy and puerperium: review of 67 cases. Stroke 1993;24:1880-4 3. Lanska DJ, Kryskio RJ. Risk factors for peripartum and postpartum stroke and intracranial venous thrombosis. Stroke 2000;31:1274-82 4. Ferro JM, Canhao P, Stam J, Bousser MG, Barinagarrementeria F. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke 2004;35:664-70 5. Lamy C, Hamon JB, Coste J, Mas JL. Ischemic stroke in young women: risk of recurrence during subsequent pregnancies. French Study Group on Stroke in Pregnancy. Neurology. 2000;55:269-74. 6. Dentali F, Gianni M, Crowther MA, Ageno W. Natural history of cerebral vein thrombosis: a systematic review. Blood, 15 2006;108:1129-34 haematologica/the hematology journal | 2007; 92(s1) | 305
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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
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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
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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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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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
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Page 287 and 288: modulated after 24 h (37 up- and 59
Page 289 and 290: 0753 A SUSTAINED REMISSION OF IDIOP
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Page 295 and 296: Results. A total of 396 patients we
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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: 0809 CURRENT APPROACH TO CHELATION
Page 315 and 316: the 97.5th percentile (5.2 U/mL) ge
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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
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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
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without type 2 diabetes. Methods. T
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pts (38.8%) that were isolated (abs
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y using the Miltenyi CD34 isolation
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0969 COMPARISON OF CD25 IMMUNOHISTO
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cytes was 24 days (range 8-32 days)
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a cytogenetic hallmark for M4/M5 su
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normal human BM B progenitor cells
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0994 INCIDENCE OF INVASIVE ASPERGIL
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3 of disease relapse.TRM at day+100
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survival of five years. This dismal
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1011 FLOW CYTOMETRIC DNA INDEX AND
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1018 THE EFFECT OF THE SUGARBAKER P
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1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
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1063 ABNORMAL METHYLATION STATUS OF
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1069 CLINICAL RELEVANCE OF REGULATO
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1076 SERUM LEVELS OF SOLUBLE HLA CL
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patient is still undergoing intensi
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nificant MVD differences were detec
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dictor of OS (p=0.004). High dose t
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1099 ALTERATIONS IN THE NATURAL KIL
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1105 CYTOGENETIC ABNORMALITIES IN 3
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1110 CONSTITUTIVE ACTIVATION OF STA
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efficacy results with a well-tolera
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unmutated VH genes, and high and lo
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Aims. Aim of this study was to pred
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tested across a wide range of human
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were incidentally diagnosed (52%).
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ß2GP1 may be considered as determi
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characterized in 198 β thalassaemi
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
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of the drug is crucial to allow lon
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egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
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events -Postoperative states: 9,19%
Page 451 and 452:
efficacy and decreased atherosclero
Page 453 and 454:
1217 INCIDENCE OF EARLY STAGE IDIOP
Page 455 and 456:
1691GA and 1 homozygous 1691AA. The
Page 457 and 458:
1230 ASSOCIATION OF HEPARANASE GENE
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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