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  • 1.
    Andersen, Christen Lykkegaard
    et al.
    Dept Hematol, Roskilde Univ Hosp, Roskilde, Denmark..
    Bjorn, Mads Emil
    Dept Hematol, Roskilde Univ Hosp, Roskilde, Denmark..
    McMullin, Mary Frances
    Dept Haematol, Queen Univ Belfast Antrim, Belfast, North Ireland.
    Harrison, Claire
    Dept Haematol, NHS Fdn Trust, London, England.
    Samuelsson, Jan
    Dept Internal Med, Stockholm South Hosp, Stockholm, Sweden..
    Ejerblad, Elisabeth
    Dept Hematol, Univ Uppsala Hosp, Uppsala, Sweden..
    Zweegman, Sonja
    Dept Hematol, Vrije Univ Med Ctr, Amsterdam, Netherlands..
    Fernandes, Savio
    Dept Haematol, Russells Hall Hosp, Dudley, England.
    Bareford, David
    Dept Haematol, Russells Hall Hosp, Dudley, England.
    Knapper, Steven
    Dept Haematol, Cardiff Univ, Cardiff, UK.
    Lofvenberg, Eva
    Hematol Ctr, Karolinska Univ Hosp, Stockholm, Sweden.
    Linder, Olle
    Dept Med, Div Hematol, Örebro Univ Hosp, Örebro, Sweden..
    Andreasson, Bjorn
    Dept Hematol, NU Hosp Org, Uddevalla Hosp, Uddevalla, Sweden.
    Ahlstrand, Erik
    Örebro University Hospital. Dept Med, Div Hematol, Örebro University Hospital, Örebro, Sweden.
    Jensen, Morten Krogh
    Dept Hematol, Herlev Hosp, Herlev, Denmark.
    Bjerrum, Ole Weis
    Dept Hematol, Copenhagen Univ Hosp, Rigshosp, Copenhagen, Denmark.
    Vestergaard, Hanne
    Dept Hematol, Odense Univ Hosp, Odense, Denmark.
    Larsen, Herdis
    Dept Hematol, Dept Internal Med, Viborg Hosp, Viborg, Denmark.
    Klausen, Tobias Wirenfeldt
    Dept Hematol,Herlev Hosp, Herlev, Denmark.
    Mourits-Andersen, Torben
    Dept Hematol, Esbjerg Cent Hosp, Esbjerg, Denmark.
    Skov, Vibe
    Dept Clin Genet, Odense Univ Hosp, Odense, Denmark.
    Thomassen, Mads
    Dept Clin Genet, Odense Univ Hosp, Odense, Denmark.
    Kruse, Torben
    Dept Clin Genet, Odense Univ Hosp, Odense, Denmark.
    Gronbaek, Kirsten
    Dept Hematol, Copenhagen Univ Hosp, Rigshosp, Copenhagen, Denmark.
    Hasselbalch, Hans Carl
    Dept Hematol, Roskilde Univ Hosp, Roskilde, Denmark.
    Circulating YKL-40 in patients with essential thrombocythemia and polycythemia vera treated with the novel histone deacetylase inhibitor vorinostat2014In: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 38, no 7, p. 816-821Article in journal (Refereed)
    Abstract [en]

    YKL-40 regulates vascular endothelial growth factors and induces tumor proliferation. We investigated YKL-40 before and after treatment with vorinostat in 31 polycythemia vera (PV) and 16 essential thrombocythemia (ET) patients. Baseline PV patient levels were 2 times higher than in healthy controls (P<0.0001) and 1.7 times higher than in ET (P = 0.02). A significant correlation between YKL-40 at baseline and neutrophils, CRP, LDH, JAK2V617F and platelets in PV patients was observed, as well as a significantly greater reduction of YKL-40 levels in PV patients responding to therapy. YKL-40 might be a novel marker of disease burden and progression in myeloproliferative neoplasms.

  • 2.
    Ekbäck, Maria [Palmetun]
    et al.
    Department of Dermatology, Örebro University Hospital, Örebro, Sweden; Department of Medicine, Örebro University, Örebro, Sweden.
    Uggla, Bertil
    Department of Internal Medicine, Örebro University Hospital, Örebro, Sweden.
    Paraneoplastic pemphigus associated with chronic lymphocytic leukaemia: treatment with alemtuzumab2012In: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 36, no 8, p. E190-E191Article in journal (Refereed)
  • 3.
    Fergedal, May
    et al.
    Department of Pathology, Örebro Medical Center Hospital, Örebro, Sweden.
    Åström, Maria
    Department of Internal Medicine, Örebro Medical Center Hospital, Örebro, Sweden.
    Tidefelt, Ulf
    Department of Internal Medicine, Örebro Medical Center Hospital, Örebro, Sweden.
    Karlsson, Mats G.
    Department of Pathology, Örebro Medical Center Hospital, Örebro, Sweden.
    Differences in CD14 and alpha-naphthyl acetate esterase positivity and relation to prognosis in AML1998In: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 22, no 1, p. 25-30Article in journal (Refereed)
    Abstract [en]

    Alpha-naphthyl acetate esterase (ANAE) and CD14 expression, used for determination of monocytic cells, were compared and related to prognosis in 65 AML patients. Bone marrow aspiration material from AML patients has been used for the cytochemistry as well as flow cytometry. All non-erythroid cells have been included in the evaluation in both methods. 17/65 cases showed at least 15% difference between the proportion CD14 and ANAE positive cells. Cases with 20% or more CD14 positivity had poorer prognosis. For FAB classes M0-M3, presence of 10% or more CD14 was negative for overall survival (P = 0.01). ANAE did not show significant prognostic influence.

  • 4.
    Uggla, Bertil
    et al.
    Department of Medicine, Örebro Medical Center Hospital, Örebro, Sweden.
    Möllgård, Lars
    Department of Hematology, Huddinge Uniersity Hospital, Huddinge, Sweden.
    Ståhl, Elisabeth
    Department of Pathology, Örebro Medical Center Hospital, Örebro, Sweden.
    Mossberg, Lise-Lott Mossberg
    Department of Pathology, Örebro Medical Center Hospital, Örebro, Sweden.
    Karlsson, Mats G.
    Department of Pathology, Örebro Medical Center Hospital, Örebro, Sweden.
    Paul, Christer
    Department of Pathology, Örebro Medical Center Hospital, Örebro, Sweden; Karolinska Institute, Stockholm, Sweden.
    Tidefelt, Ulf
    Department of Medicine, Örebro Medical Center Hospital, Örebro, Sweden; Karolinska Institute, Stockholm, Sweden.
    Expression of topoisomerase IIalpha in the G0/G1 cell cycle phase of fresh leukemic cells2001In: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 25, no 11, p. 961-966Article in journal (Refereed)
    Abstract [en]

    Topoisomerase IIalpha (topoII alpha) is the target enzyme for several antineoplastic drugs. Correlation between low expression of topo IIalpha and drug resistance has been shown in vitro, but there is limited evidence of a correlation to initial response to treatment or to overall prognosis. Normal cells express topo IIalpha in S/G2/M phase of the cell cycle but not in G0/G1 phase. However, some data suggest that topo IIalpha could be expressed in G0/G1 phase in malignant cells. We have investigated the expression of topo IIalpha in leukemic cells from 25 patients with acute leukemia by flow cytometry, separating cells of different cell cycle phases. We demonstrated that 9/25 samples showed >50% positive cells in G0/G1, and another five samples showed >20%. This finding could possibly provide an explanation to previous difficulties in correlating topo IIalpha expression with clinical outcome. Six of eight patients, where >20% of the cells in G0/G1 were positive for topo IIalpha, entered CR, compared to one of five patients with <20% topo IIalpha positive cells in G0/G1. We suggest that topo IIalpha expression in G0/G1 in leukemic cells may be of predictive value for clinical response to cytostatic drugs.

  • 5.
    Uggla, Bertil
    et al.
    Department of Medicine, Örebro University Hospital, Örebro; Karolinska Institute, Stockholm.
    Ståhl, Elisabet
    Clinical Research Centre, Örebro University Hospital, Örebro.
    Wågsäter, Dick
    Örebro University, Department of Nursing and Caring Sciences.
    Paul, Christer
    Department of Haematology, Huddinge University Hospital, Stockholm; Karolinska Institute, Stockholm.
    Karlsson, Mats G.
    Department of Pathology, Örebro University Hospital, Örebro.
    Sirsjö, Allan
    Örebro University, Department of Nursing and Caring Sciences.
    Tidefelt, Ulf
    Örebro University, Department of Clinical Medicine. Department of Medicine, Örebro University Hospital, Örebro.
    BCRP mRNA expression v. clinical outcome in 40 adult AML patients2005In: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 29, no 2, p. 141-146Article in journal (Refereed)
    Abstract [en]

    Efflux pumps are considered being mechanisms behind drug resistance in acute myeloid leukaemia (AML). A recently described efflux pump, breast cancer resistance protein (BCRP), can be expressed in AML, but its clinical importance is uncertain. In this study BCRP mRNA expression was determined in samples from 40 AML patients by real-time RT-PCR. The expression varied from negative to 76 times that of control cells. There was no difference in BCRP mRNA expression between patients responding to induction treatment and non-responders. However, in the group of responders, the 14 patients with the highest expression had significantly shorter overall survival (mean 38 months, SEM 15 months) than the 14 patients with the lowest (74 months, SEM 16 months) (P = 0.047). This suggests a possible role of BCRP in drug resistance in AML.

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