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  • 151. Tierens, Anne
    et al.
    Bjørklund, Elizabeth
    Siitonen, Sanna
    Marquart, Hanne Vibeke
    Wulff-Juergensen, Gitte
    Pelliniemi, Tarja-Terttu
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Hasle, Henrik
    Jahnukainen, Kirsi
    Lausen, Birgitte
    Jonsson, Olafur G.
    Palle, Josefine
    Zeller, Bem
    Fogelstrand, Linda
    Abrahamsson, Jonas
    Residual disease detected by flow cytometry is an independent predictor of survival in childhood acute myeloid leukaemia; results of the NOPHO-AML 2004 study2016Ingår i: British Journal of Haematology, ISSN 0007-1048, E-ISSN 1365-2141, Vol. 174, nr 4, s. 600-609Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Early response after induction is a prognostic factor for disease outcome in childhood acute myeloid leukaemia (AML). Residual disease (RD) detection by multiparameter flow cytometry (MFC) was performed at day 15 and before consolidation therapy in 101 patients enrolled in the Nordic Society of Paediatric Haemato-Oncology AML 2004 study. A multicentre laboratory approach to RD analysis was used. Event-free survival (EFS) and overall survival (OS) was significantly different in patients with and without RD at both time points, using a 0.1% RD cut-off level. RD-negative and -positive patients after first induction showed a 5-year EFS of 65.7% and 22.7%, respectively (P < 0.001) and an OS of 77.6% (P = 0.025) and 51.8%. RD-negative and -positive patients at start of consolidation therapy had a 5-year EFS of 57.7% and 11.7%, respectively (P < 0001) and an OS of 786% and 2811%) (P < 0001). In multivariate analysis only RD was significantly correlated with survival. RD before consolidation therapy was the strongest independent prognostic factor for EFS [hazard ratio (HR): 5.0; 95% confidence interval (CI): 1.9-133] and OS (HR: 7.0; 95% CI: 20-245). In conclusion, RD before consolidation therapy identifies patients at high risk of relapse in need of intensified treatment. In addition, RD detection can be performed in a multicentre setting and can be implemented in future trials.

  • 152. Toft, N.
    et al.
    Birgens, H.
    Abrahamsson, J.
    Griskevicius, L.
    Hallbook, H.
    Heyman, M.
    Klausen, T. W.
    Jonsson, O. G.
    Palk, K.
    Pruunsild, K.
    Quist-Paulsen, P.
    Vaitkeviciene, G.
    Vettenranta, K.
    Asberg, A.
    Frandsen, T. Leth
    Marquart, H. V.
    Madsen, H. O.
    Norén-Nyström, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Schmiegelow, K.
    ADULTS AND CHILDREN (1-45 YEARS) WITH PH-NEGATIVE ALL HAVE ALMOST IDENTICAL OUTCOME IN RISK-STRATIFIED ANALYSIS OF NOPHO ALL20082016Ingår i: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 101, s. 35-35Artikel i tidskrift (Övrigt vetenskapligt)
  • 153. Toft, N.
    et al.
    Birgens, H.
    Abrahamsson, J.
    Griskevicius, L.
    Hallböök, H.
    Heyman, M.
    Klausen, T. W.
    Jónsson, O. G.
    Palk, K.
    Pruunsild, K.
    Quist-Paulsen, P.
    Vaitkeviciene, G.
    Vettenranta, K.
    Åsberg, A.
    Frandsen, T. L.
    Marquart, H. V.
    Madsen, H. O.
    Norén-Nyström, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Schmiegelow, K.
    Results of NOPHO ALL2008 treatment for patients aged 1-45 years with acute lymphoblastic leukemia2018Ingår i: Leukemia, ISSN 0887-6924, E-ISSN 1476-5551, Vol. 32, nr 3, s. 606-615Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Adults with acute lymphoblastic leukemia (ALL) do worse than children. From 7/2008 to 12/2014, Nordic and Baltic centers treated 1509 consecutive patients aged 1-45 years with Philadelphia chromosome-negative ALL according to the NOPHO ALL2008 without cranial irradiation. Overall, 1022 patients were of age 1-9 years (A), 266 were 10-17 years (B) and 221 were 18-45 years (C). Sixteen patients (three adults) died during induction. All others achieved remission after induction or 1-3 intensive blocks. Subsequently, 45 patients (12 adults) died, 122 patients relapsed (32 adults) with a median time to relapse of 1.6 years and 13 (no adult) developed a second malignancy. Median follow-up time was 4.6 years. Among the three age groups, older patients more often had higher risk ALL due to T-ALL (32%/25%/9%, P<0.001), KMT2A rearrangements (6%/5%/3%, P<0.001) and higher day 29 residual leukemia for B-lineage (P<0.001), but not T-ALL (P = 0.53). Event-free survival rates (pEFS(5y)) were 89 +/- 1% (A), 80 +/- 3% (B) and 74 +/- 4% (C) with significant differences only for non-high risk groups. Except for thrombosis, pancreatitis and osteonecrosis, the risk of 19 specified toxicities was not enhanced by age above 10 years. In conclusion, a pediatric-based protocol is tolerable and effective for young adults, despite their increased frequency of higher risk features.

  • 154.
    Toss, Fredrik
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB). Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Edgren, Gustaf
    Berlin, Gösta
    Stegmayr, Bernd
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Witt, Volker
    Does prophylactic calcium in apheresis cause more harm than good?: Centre heterogeneity within the World Apheresis Association Register prevents firm conclusions2018Ingår i: Vox Sanguinis, ISSN 0042-9007, E-ISSN 1423-0410, Vol. 113, nr 7, s. 632-638Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background and objectives: Symptomatic hypocalcaemia is common during apheresis procedures based on citrate‐based anticoagulants. As a consequence, patients often receive prophylactic calcium treatment. However, a recent publication based on the World Apheresis Association (WAA) register suggested harmful effects of such prophylactic calcium use. Recognizing possible limitations in the previous WAA register analyses, we critically re‐evaluate the data, to test whether a change in prophylactic calcium usage may be warranted.

    Materials and methods: Using the WAA register, we reanalysed previous data by means of centre and treatment type stratification, to explore the role of prophylactic calcium as a risk factor for adverse events.

    Results: There was large variability in adverse event rates dependent on the centre performing the apheresis procedure and dependent on the type of procedure. When this variability was accounted for, there was no clear effect of calcium administration on risk of adverse effects.

    Conclusion: Shortcomings in the previous WAA register analyses may have failed to account for important confounding factors resulting in a substantial overestimation of the risk attributable to calcium usage. Overall our findings do not support a negative effect of prophylactic calcium administration in the apheresis setting.

  • 155. Ueda, Yasutaka
    et al.
    Calado, Rodrigo T.
    Norberg, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Kajigaya, Sachiko
    Roos, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Hellstrom-Lindberg, Eva
    Young, Neal S.
    A mutation in the H/ACA box of telomerase RNA component gene (TERC) in a young patient with myelodysplastic syndrome2014Ingår i: BMC Medical Genetics, ISSN 1471-2350, E-ISSN 1471-2350, Vol. 15, s. 68-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Telomeres are repeated sequences (the hexanucleotide TTAGGG in vertebrates) located at chromosome ends of eukaryotes, protecting DNA from end joining or degradation. Telomeres become shorter with each cell cycle, but telomerase, a ribonucleoprotein complex, alleviates this attrition. The telomerase RNA component (TERC) is an essential element of telomerase, serving as a template for telomere elongation. The H/ACA domain of TERC is indispensable for telomere biogenesis. Mutations in the telomerase components allow accelerated telomere loss, resulting in various disease manifestations, including bone marrow failure. To date, this is the first detailed report of an H-box mutation in TERC that is related to human disease. Case presentation: A 26-year-old man with myelodysplastic syndrome (MDS) had very short telomeres. Sequencing identified a single heterozygous mutation in the H box of the patient's TERC gene. The same mutation was also present in his father and his son, demonstrating that it was germline in origin. The telomere length in the father's blood was shorter compared to age-matched healthy controls, while it was normal in the son and also in the sperm cells of the patient. In vitro experiments suggested that the mutation was responsible for the telomere shortening in the patient's leukocytes and contributed to the pathogenesis of bone marrow failure in our patient. Conclusion: We analyzed a mutation (A377G) in the H box of TERC in a young MDS patient who had significantly short-for-age telomeres. As telomeres protect chromosomes from instability, it is highly plausible that this genetic lesion was responsible for the patient's hematological manifestations, including marrow failure and aneuploidy in the hematopoietic stem cell compartment.

  • 156.
    Wahlin, Anders
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Billström, Rolf
    Björ, Ove
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Ahlgren, Tomas
    Hedenus, Michael
    Höglund, Martin
    Lindmark, Anders
    Markevärn, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Nilsson, Bo
    Sallerfors, Bengt
    Brune, Mats
    Results of risk-adapted therapy in acute myeloid leukaemia. A long-term population-based follow-up study2009Ingår i: European Journal of Haematology, ISSN 0902-4441, E-ISSN 1600-0609, Vol. 83, nr 2, s. 99-107Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In 1997-2003, a protocol for treatment of acute myeloid leukaemia (AML) (except promyelocytic leukaemia) was activated in four Swedish health care regions covering 50% of the national population. Based on cytogenetics and clinical findings, patients aged 18-60 yr were assigned to one of three risk groups. In this report we account for the long-term clinical outcome of enrolled patients. Patients received idarubicin and cytarabine in standard doses as induction therapy and consolidation courses included high-dose cytarabine. Allogeneic stem cell transplantation (allo-SCT) from an human leucocyte antigen-identical sibling was recommended in standard and poor-risk patients, whereas unrelated donor transplant was reserved for poor-risk patients. Autologous (auto-SCT) was optional for standard or poor risk patients not eligible for allo-SCT. Two hundred seventy-nine patients with de novo or secondary (9%) AML, median age 51 (18-60) yr, corresponding to 77% of all patients in the population, were included. Twenty (7%) patients were assigned to the good risk group, whereas 150 (54%) and 109 patients (39%) were assigned to standard- and poor-risk groups, respectively. Induction failures accounted for 55 patients; 16 early deaths eight of whom had white blood cell (WBC) >100 at diagnosis, and 39 refractory disease. Thus, complete remission (CR) rate was 80%. At study closure, the median follow-up time of living patients was 90 months. Median survival time from diagnosis in the whole group was 27 months and 4-yr overall survival (OS) rate was 44%. In good, standard, and poor risk groups, 4-yr OS rates were 60, 57 and 24%, respectively. Median relapse-free survival (RFS) time in CR1 was 25 months and RFS at 4 yr was 44%. Four-year RFS rates were significantly (P < 0.001) different between the three risk groups; 64% in good risk, 51% in standard risk and 27% in poor risk patients. One hundred-ten transplantations were performed in CR1; 74 allo-SCT (50 sibling, 24 unrelated donor), and 36 auto-SCT. Non-relapse mortality was 16% for allo-SCT patients. Outcome after relapse was poor with median time to death 163 d and 4-yr survival rate 17%. Three conclusions were: (i) these data reflect treatment results in a minimally selected population-based cohort of adult AML patients <60 yr old; (ii) a risk-adapted therapy aiming at early allogeneic SCT in patients with a high risk of relapse is hampered by induction deaths, refractory disease, and early relapses; and (iii) high WBC count at diagnosis is confirmed as a strong risk factor for early death but not for relapse.

  • 157. Wahlin, B. E.
    et al.
    Overgaard, N.
    Peterson, S.
    Digkas, E.
    Glimelius, I.
    Lagerlof, I.
    Johansson, Ann-Sofie
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Palma, M.
    Hansson, L.
    Linderoth, J.
    Goldkuhl, C.
    Molin, D.
    HODGKIN LYMPHOMA IN SWEDEN SINCE 2000: BETTER SURVIVAL ONLY IN ELDERLY WOMEN - A SWEDISH LYMPHOMA REGISTRY STUDY2016Ingår i: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 101, nr S5, s. 22-22, artikel-id P005Artikel i tidskrift (Refereegranskat)
  • 158. Wareham, N. E.
    et al.
    Heilmann, C.
    Abrahamsson, J.
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap.
    Gustafsson, B.
    Ha, S-Y
    Heldrup, J.
    Jahnukainen, K.
    Jonsson, O. G.
    Lausen, B.
    Palle, J.
    Zeller, B.
    Hasle, H.
    Outcome of poor response paediatric AML using early SCT2012Ingår i: Biology of blood and marrow transplantation, ISSN 1083-8791, E-ISSN 1523-6536, Vol. 18, nr 2, s. S235-S235Artikel i tidskrift (Övrigt vetenskapligt)
  • 159. Wareham, Neval E.
    et al.
    Heilmann, Carsten
    Abrahamsson, Jonas
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Gustafsson, Britt
    Ha, Shau-Yin
    Heldrup, Jesper
    Jahnukainen, Kirsi
    Jonsson, Olafur G.
    Lausen, Birgitte
    Palle, Josefine
    Zeller, Bernward
    Hasle, Henrik
    Outcome of poor response paediatric AML using early SCT2013Ingår i: European Journal of Haematology, ISSN 0902-4441, E-ISSN 1600-0609, Vol. 90, nr 3, s. 187-194Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background Children with poor response acute myeloid leukaemia (AML) generally have a very poor outcome. Allogeneic stem cell transplantation (SCT) is often recommended for these children but the benefit is unclear. The aim of this study was to investigate survival for poor response AML patients treated with SCT. Material and Methods Treatment was given according to the NOPHO-AML 2004 protocol. All patients received AIET (Cytarabine, Idarubicin, Etoposide, Thioguanine) and AM (Cytarabine, Mitoxantrone) as induction. We included poor response defined as > 15% blasts on day 15 after AIET (n=17) or > 5% blasts after AM (n=14, refractory disease). Poor response patients received intensively timed induction and proceeded to SCT when a donor was available. Results Thirty-one of 267 evaluable patients (12%) had a poor response. SCT was performed in 25; using matched unrelated donors in 13, matched sibling donors in 6, cord blood donor in 4, and haploidentical donor in two. The median follow-up for the 31 poor responding patients was 2.6 years (range 0.4 - 8.1 years) and 3-year probability of survival 70% (95% CI 59-77%). Conclusions The poor responders in the NOPHO-AML 2004 protocol had a favourable prognosis treated with time-intensive induction followed by SCT.

  • 160. Wennström, Lovisa
    et al.
    Edslev, Pernille Wendtland
    Abrahamsson, Jonas
    Nørgaard, Jan Maxwell
    Fløisand, Yngvar
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Gustafsson, Göran
    Heldrup, Jesper
    Hovi, Liisa
    Jahnukainen, Kirsi
    Jonsson, Olafur Gisli
    Lausen, Birgitte
    Palle, Josefine
    Zeller, Bernward
    Holmberg, Erik
    Juliusson, Gunnar
    Stockelberg, Dick
    Hasle, Henrik
    Acute Myeloid Leukemia in Adolescents and Young Adults Treated in Pediatric and Adult Departments in the Nordic Countries2016Ingår i: Pediatric Blood & Cancer, ISSN 1545-5009, E-ISSN 1545-5017, Vol. 63, nr 1, s. 83-92Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Studies on adolescents and young adults with acute lymphoblastic leukemia suggest better results when using pediatric protocols for adult patients, while corresponding data for acute myeloid leukemia (AML) are limited. Procedure: We investigated disease characteristics and outcome for de novo AML patients 10-30 years old treated in pediatric or adult departments. We included 166 patients 10-18 years of age with AML treated according to the pediatric NOPHO-protocols (1993-2009) compared with 253 patients aged 15-30 years treated in hematology departments (1996-2009) in the Nordic countries. Results: The incidence of AML was 4.9/million/year for the age group 10-14 years, 6.5 for 15-18 years, and 6.9 for 19-30 years. Acute promyelocytic leukemia (APL) was more frequent in adults and in females of all ages. Pediatric patients with APL had similar overall survival as pediatric patients without APL. Overall survival at 5 years was 60% (52-68%) for pediatric patients compared to 65% (58-70%) for adult patients. Cytogenetics and presenting white blood cell count were the only independent prognostic factors for overall survival. Age was not an independent prognostic factor. Conclusions: No difference was found in outcome for AML patients age 10-30 years treated according to pediatric as compared to adult protocols.

  • 161. Winqvist, Maria
    et al.
    Andersson, Per-Ola
    Asklid, Anna
    Karlsson, Karin
    Karlsson, Claes
    Lauri, Birgitta
    Lundin, Jeanette
    Mattsson, Mattias
    Norin, Stefan
    Sandstedt, Anna
    Rosenquist, Richard
    Späth, Florentin
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hansson, Lotta
    Österborg, Anders
    Long-term real-world results of ibrutinib therapy in patients with relapsed or refractory chronic lymphocytic leukemia: 30-month follow up of the Swedish compassionate use cohort2019Ingår i: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 104, nr 5, s. E208-E210Artikel i tidskrift (Refereegranskat)
  • 162. Yektaei, Elham
    et al.
    Nilsson, Anders
    Nasman-Glaser, Barbro
    Ekblom, Marja
    Qian, Hong
    Radmark, Olof
    Zovko, Ana
    Kanter, Lena
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Stenke, Leif
    Modulation of Leukotriene Signaling Affecting Cell Growth in Chronic Myeloid Leukemia: A Key Pathway to Cure?2015Ingår i: Blood, ISSN 0006-4971, E-ISSN 1528-0020, Vol. 126, nr 23Artikel i tidskrift (Övrigt vetenskapligt)
  • 163. Yektaei-Karin, Elham
    et al.
    Zovko, Ana
    Nilsson, Anders
    Näsman-Glaser, Barbro
    Kanter, Lena
    Rådmark, Olof
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Ekblom, Marja
    Dolinska, Monika
    Qian, Hong
    Stenke, Leif
    Modulation of leukotriene signaling inhibiting cell growth in chronic myeloid leukemia2017Ingår i: Leukemia and Lymphoma, ISSN 1042-8194, E-ISSN 1029-2403, Vol. 58, nr 8, s. 1903-1913Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Although tyrosine kinase inhibitors (TKIs) have dramatically improved clinical outcome in chronic myeloid leukemia (CML), cure rarely occurs. This may be due to BCR-ABL-independent, aberrant signaling pathways, one of which leads to leukotriene (LT) formation. Well-recognized as inflammatory mediators, LT can also affect oncogenic mechanisms of several tumors. We have previously discovered elevated LT-synthesis and up-regulated cysteinyl-LT-inducing enzyme in CML. Here we report on dose-dependent inhibition of CML cell growth exerted by specific blockers of LT-signaling. Thus, the cysteinyl-LT1-receptor-antagonist montelukast significantly reduced the growth of K562, KCL22, and KU812 cells, as well as primary CD34(+) blood cells from two CML patients. Adding montelukast to the TKI imatinib caused combined inhibition. No effect was seen on normal bone marrow cells. Similarly, growth inhibition was also observed with the 5-lipoxygenase (LO)-inhibitor BWA4C, the 5-LO-activating-protein-(FLAP)-inhibitor licofelone and the LTB4(BLT1)-receptor-antagonist LY293111. Thus, blocking of aberrant LT-signaling may provide an additional, novel therapeutic possibility in CML.

  • 164.
    Zachariadis, V
    et al.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Gauffin, F
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Kuchinskaya, E
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Heyman, M
    Department of Woman and Child Health, Karolinska Institutet, Stockholm, Sweden.
    Schoumans, J
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Blennow, E
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Gustafsson, B
    Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
    Barbany, G
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Golovleva, Irina
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Ehrencrona, H
    Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden.
    Cavelier, L
    Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden.
    Palmqvist, L
    Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
    Lönnerholm, G
    Department of Women's and Children's Health, University Children's Hospital, Uppsala, Sweden.
    Nordenskjöld, M
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Johansson, B
    Department of Clinical Genetics, University and Regional Laboratories, Skåne University Hospital, Lund University, Lund, Sweden.
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Nordgren, A
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    The frequency and prognostic impact of dic(9;20)(p13.2;q11.2) in childhood B-cell precursor acute lymphoblastic leukemia: results from the NOPHO ALL-2000 trial2011Ingår i: Leukemia, ISSN 0887-6924, E-ISSN 1476-5551, Vol. 25, nr 4, s. 622-628Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The dic(9;20)(p13.2;q11.2) is reported to be present in ∼2% of childhood B-cell precursor acute lymphoblastic leukemia (BCP ALL). However, it easily escapes detection by G-banding analysis and its true prevalence is hence unknown. We performed interphase fluorescence in situ hybridization analyses-in a three-step manner-using probes for: (i) CDKN2A at 9p21, (ii) 20p and 20q subtelomeres and (iii) cen9 and cen20. Out of 1033 BCP ALLs diagnosed from 2001 to 2006, 533 were analyzed; 16% (84/533) displayed 9p21 deletions, of which 30% (25/84) had dic(9;20). Thus, dic(9;20)-positivity was found in 4.7% (25/533), making it the third most common genetic subgroup after high hyperdiploidy and t(12;21)(p13;q22). The dic(9;20) was associated with a female predominance and an age peak at 3 years; 18/25 (72%) were allocated to non-standard risk treatment at diagnosis. Including cases detected by G-banding alone, 29 dic(9;20)-positive cases were treated according to the NOPHO ALL 2000 protocol. Relapses occurred in 24% (7/29) resulting in a 5-year event-free survival of 0.69, which was significantly worse than for t(12;21) (0.87; P=0.002) and high hyperdiploidy (0.82; P=0.04). We conclude that dic(9;20) is twice as common as previously surmised, with many cases going undetected by G-banding analysis, and that dic(9;20) should be considered a non-standard risk abnormality.

  • 165. Zachariadis, V.
    et al.
    Schoumans, J.
    Ofverholm, I.
    Barbany, G.
    Halvardsson, E.
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Johansson, B.
    Nordenskjold, M.
    Nordgren, A.
    Detecting dic(9;20)(p13.2;p11.2)-positive B-cell precursor acute lymphoblastic leukemia in a clinical setting using fluorescence in situ hybridization2014Ingår i: Leukemia, ISSN 0887-6924, E-ISSN 1476-5551, Vol. 28, nr 1, s. 196-198Artikel i tidskrift (Refereegranskat)
  • 166. Zachariadis, Vasilios
    et al.
    Schoumans, Jacqueline
    Barbany, Gisela
    Heyman, Mats
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Johansson, Bertil
    Nordenskjöld, Magnus
    Nordgren, Ann
    Homozygous deletions of CDKN2A are present in all dic(9;20)(p13.2;q11.2)-positive B-cell precursor acute lymphoblastic leukaemias and may be important for leukaemic transformation2012Ingår i: British Journal of Haematology, ISSN 0007-1048, E-ISSN 1365-2141, Vol. 159, nr 4, s. 488-491Artikel i tidskrift (Refereegranskat)
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