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12 th Congress of the European Hematology Association MPDs. We studied 17 patients with MPDs, 9 of them experienced ET, 5 PV and 3 IMF. Results. 7 out of 9 patients with ET, 1 out of 2 patients with PV and 2 out of 3 patients with IMF were JAK 2 V617F positive. We found that the patients who were positive for the V617F mutation had also increased levels of VEGF in both serum and immunohistochemical proportions of bone marrow, compared to the MPD patients with the JAK2 wild type. Higher levels of VEGF in both the serum and bone marrow were found in MPD patients than in controls. The statistical analysis showed that, in patients with JAK2 wild type, the mean±SD level of serum VEGF was calculated 639±594.3 pg/mL, whereas in JAK2 V617F patients, the serum VEGF level was 1001±528.4 pg/mL. The medial levels for VEGF in serum were 539 pg/mL for the JAK2 wild type patients and 866 pg/mL for the JAK2 V617F patients. Regarding the immunohistochemical VEGF expression in bone marrow, the mean±SD level was counted 23.75± 10.3% for the patients with JAK2 wild type and in JAK2 V617F patients the mean level was 37.14± 9.9%. The median levels were 20% for the JAK2 wild type patients and 30% for the JAK2 V617F patients. Conclusions. These results are suggestive of an important role of angiogenesis and apoptosis in MPDs. Those two procedures are likely to influence each other and we are not yet sure which of those events is the promoter for the other. It also seems that they play a crucial role in the pathogenesis and prognosis as well as in the duration of the diseases and transformation to acute leukemia. They probably are two of the key points towards the therapeutic options of MPDs. This finding puts forward the use of targeted therapies, such as anti- VEGF antibodies in MPD patients. 1552 RECLASSIFICATION OF HAEMATOLOGICAL MALIGNANCIES ACCORDING MORPHOLOGY DATA M. Giraldo, 1 P. Latre, 2 E. Franco-García, 3 R. Alvarez, 4 J. Pascual, 4 C. Martos5 1 Miguel Servet University Hospital, ZARAGOZA; 2 FEETEG, ZARAGOZA, Spain; 3 FEHHA, ZARAGOZA; 4 Hospital U Miguel Servet, ZARAGOZA; 5 Aragon Health Department, ZARAGOZA, Spain Background and Aims. Related to the HAEMACARE project we pretend revise the codes of Zaragoza population cancer registry in order to increase availability and standardisation of morphology data, ensuring a strict adherence to ICD-O classification assess the distribution of the haematological malignancies as lymphoid neoplasms, acute and chronic myeloid leukaemias and multiple myeloma. Patients and Method. From January 1996 to December 2000, 2,852 patients diagnosed with haematological malignancies were recruited from different sources: the population-based Cancer Registry of Zaragoza, Registry of haematological malignancies of FEHHA and Miguel Servet Hospital records. Former pathological and hematological diagnoses were reviewed and some were prospectively reclassified following the latest WHO classification and their histological subtypes in accordance with the World Health Organization (WHO) classification. We have estimate survival according to specific morphology groups. Results. Following criteria established by WHO classification the distribution of lymphoid neoplasms was as follows: B-cell neoplasm 64.5%, T-cell neoplasm 3.3%, Hodgkin lymphoma 4.1%; Myelodisplastic syndromes 9.9%, acute lymphoblastic leukaemia 1.9%, acute myeloid leukaemia 4.0%, chronic myeloid leukaemia 2.3% and multiple myeloma 10.0%. Diffuse large B-cell lymphoma (13.5%) and chronic B lymphoid leukaemia (9.3%) showed the highest incidence rate in adults. Conclusions. A higher incidence rate of lymphoid neoplasms was found in men in our area. We have observed in the last period of study a tendency of survival differences. 548 | haematologica/the hematology journal | 2007; 92(s1)
Index of authors A Aapro, M., 0377, 1206 Abad, M.T., 1147 Abbas, R., 0321 Abbruzzese, L., 0506 Abd El Hamid, A., 1514 Abd El Rahaman, M, 1535 Abdallah, A., 0575 Abdallah, M., 0146 Abdel Aziz, F., 1514 Abdelkefi, A., 0988, 1236 Abdelrazik, N., 0960, 1146, 1389, 1408 Abdel-Razik, M., 1405 Abdelsalam, M., 0950 Abd-Elwahaab, E., 1421 Abdou, S., 1421 Abdou, M.S., 1421 Abdulkarim, K., 0412 Abedi Valugerdi, M., 0592 Abella, E., 0142, 0372, 1348, 1473 Abellaneda Molina, C., 1152 Aboul-Naga, S., 0016 Abou-Lteif, G., 0733 Abraham, I., 1206 Abraira, V., 1070 Abramenko, I., 0037, 1101, 1344 Abramowicz, M.J., 0792, 1153 Abrams, S., 0747 Abrisqueta, P., 0394, 0706, 0921 Abruzzese, E, 0140, 0549 Abuzenadah, A., 1492 Accordi, B., 0152, 0888 Acedo, A., 0748 Acevedo, M., 0356 Acinas, O., 0712 Ackermann, J., 0405, 0698 Ackerstein, A., 0366 Acosta, G., 0703, 1422 Acquatella, G., 1488 Acquaviva, C., 0367 Adam, K., 0601 Adam, R.A., 1454 Adam, Z., 0257, 0262, 0277, 1162, 1383 Adami, F., 1352 Adamo, L., 0036, 1271 Adams, J., 0211, 1120 Adams, M., 0314 Adebayo, T., 0978 Adelman, D.C., 0742 Adès, L., 0222, 0427, 0482 Adjaoud, D., 1100 Aerts, M.F.G., 0735 Afanasyev, B., 0047, 0504 Afendoulidou, K., 1374 Affenberger, S., 1335 Afifi, O.A.H.A., 1517 Agis, H., 1112 Aglietta, M., 0209, 0403 Agnelli, G., 0093 Agnelli, L., 0697, 0973 Agorasti, A., 0992, 1168 Agostini, C., 0278, 1352 Agostini, F., 1299 Agrawal, D., 0529 Agrawal, S., 0078 Ågren, L., 0315 Aguilar, M., 1269 Aguilera, C., 0680 Aguirre, M.A., 0163 Agustín, M.J., 1136, 1548 Aguzzi, C., 0756, 1191 Ahluwalia, J., 1050 Ahmed, F., 0032 Ahmed, S., 0081 Ahn, H.S., 1357 Ahn, J. S., 0056, 0256, 1119 Ahn, S., 0954 Aillaud, M.-F., 0354 Aissaoui, L., 1091, 1149, 1247, 1298 Aiuti, F., 0184 Aivado, M., 0758, 0759 Ajayi, O., 1184 Ajdukovic, R., 0236 Akan, H., 1058, 1447 Akanni, E.O., 0978 Akar, N., 0819 Akbalik, M., 1393 Akehurst, R.L., 0598 Aker, M., 0366, 0580, 0581, 0956 Akhondi, M., 0512 Akhtar, S., 0950 Akiyama, H., 0933 Akiyama, M., 0979 Aksenova, E.V., 1015, 1016, 1362 Aktas, B., 1058 Akyol, A., 1429 Akyol Erikci, A., 1237 Al Ajmi, A., 1503 Al Husain, H., 1001 Al Husseini, H., 0950 Al Jaouni, S., 1167, 1531 Al Jedani, H., 1531 Al Jefri, A., 0808 Al Zir, K., 0808 Aladle, D., 1397 Al-Ali, H.K., 0019, 0563, 1178 Alam, M., 1415 Alanoglu, G., 1033 Alarcon, J., 1176, 1177 Alavi, S., 1406 Albano, F., 0539 Albarello, A., 0049, 1538 Albayrak, D., 1393 Albayrak, M., 1392, 1522 Alberca, M., 0328 Albergoni, M.P., 1024 Alberti, M., 0765 Albiero, E., 1129 Albizua, Q., 0668, 1201 Albo, C., 1036 Albuquerque, D.M., 0810, 1495 Alcaraz, S., 0703, 1422 Alcoba, E., 0703, 1422 Alcoceba, M., 0174, 0367, 0699 Aldaniarova, B., 1367 Aldrighetti, L., 0196 Alegre, A., 0404 Aleinikova, V., 1098 Alemayehou, M., 0796 Ales, M., 1187 12 th Congress of the European Hematology Association Alesiani, F., 0674 Åleskog, A., 0317 Alessandrino, E.P., 0729 Aletra, V., 0796 Alexander, H.D., 0101, 0519, 1037, 1307, 1308 Alexandraki, R., 1465 Alexandrakis, M.G, 0182, 1465 Alfonsi, M., 0666 Algarra, L., 0215 Alguel, G., 0349, 0574, 0880 Al-Harbi, A., 1492 Alietti, A., 1057 Alimena, G., 0554, 0906 Alimoghadam, K., 0943 Alioglu, B., 0342, 0345 Aljassem, L., 0222, 0427 Al-Khazraji, A., 0175 Alkindi, S., 1333 Allen, C.G., 0053 Allio, M. ., 0605 Allione, B., 0209, 0403 Allouche, H., 0988 Alloush, H., 1346 Almeida, H., 1160 Almeida Parra, J., 0206, 0328, 0577 Alonso, D., 0748 Alonso, E., 1137 Alonso, J., 0305 Al-Othman, S., 1001 Al-Qahtni, M., 1492 Al-Says, F., 1492 Alterini, R., 0301, 1218, 1453, 1497 Altés, A., 0781 Altintas, A., 0637, 0749, 0937, 1141, 1219, 1316, 1402, 1404 Altintas, S., 0768 Al-Tonbary, Y., 1405 Altuntas, F., 1055, 1469, 1472 Alvarez, R., 1304, 1552 Alvarez-Larrán, A., 0304, 0646 Alvaro, T., 1208 Alves, J., 1262 Alves, S., 0025 Alves, V., 1131 Amabile, M., 0006, 0140, 0549, 0550, 0559, 0561, 0562, 0906 Amadori, S., 0031, 0058, 0361, 0486, 0494, 0620, 1227, 1299 Amar, A., 0366 Amarante-Mendes, G.P., 0528 Amariglio, N., 0038, 0655, 0893, 1435 Amato, B., 0201 Amato, G., 0261 Amberger, A., 1077 Ambrosetti, A., 0121, 0866 Ambrósio, A.P., 0246 Amess, J., 0627 Amian, A., 1144 Amigo Garcia, V., 1314, 1550 Amin, I., 1267 Amiot, L., 0272 Ammatuna, E., 0031, 0058, 0361, 0486, 1299 Amodeo, M., 1007 haematologica/the hematology journal | 2007; 92(s1) | a
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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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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
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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
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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
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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
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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%
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efficacy and decreased atherosclero
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1217 INCIDENCE OF EARLY STAGE IDIOP
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1691GA and 1 homozygous 1691AA. The
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1230 ASSOCIATION OF HEPARANASE GENE
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posed, was: DF = (CD43%+FMC7%+CD79b
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treatment of acute promyelocityc le
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loaded group and 35 (70%) were non-
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mild. Fas and soluble Fas ligand le
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1265 POSACONAZOLE THERAPY IN REFRAC
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ly express the cytoplasmic (inactiv
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findings confirmed the significant
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a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
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1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
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phamide 750 mg/m 2 on day 1, vincri
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nomenon is unclear. It has been sug
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oped mild thrombocytopenia (platele
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gle dose of 54mg/m 2 rituximab furt
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patients (pts), 36 male, with acute
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esulting alterations of the endothe
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(range 1-7) and 28,6% of patients h
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three decades. In vivo, Ara-C is tr
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statistical analysis. Results. Seve
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Results. Though there was no recogn
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2% and 19% of patients with or with
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were older than 65 y) which can be
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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: 1548 QUALITY ANALYSIS OF THE MULTID
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
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12th Congress of the European Hematology ... - Haematologica

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