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  • 1. Gruber, A
    et al.
    Björkholm, M
    Brinch, L
    Evensen, S
    Gustavsson, B
    Hedenus, M
    Juliusson, Gunnar
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Hematologi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Hematologiska kliniken US.
    Lofvenberg, E
    Nesthus, I
    Simonsson, B
    Sjö, M
    Stenke, L
    Tangen, JM
    Tidefelt, U
    Uden, AM
    Paul, C
    Liliemark, J
    A phase I/II study of the MDR modulator Valspodar (PSC 833) combined with daunorubicin and cytarabine in patients with relapsed and primary refractory acute myeloid leukemia2003Ingår i: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 27, nr 4, s. 323-328Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The cyclosporine analog Valspodar (PSC 833, Novartis Pharma) is a strong inhibitor of the mdr1 gene product p-glycoprotein (pgp). A phase I/II study was conducted in order to evaluate if addition of Valspodar to treatment with daunorubicin and cytarabine, given to patients with primary refractory or relapsed acute myeloid leukemia, could increase the complete remission rate. Fifty-three patients were treated in cohorts of three to six patients. Twelve patients reached a complete remission in bone marrow, five of whom also normalized their peripheral blood values. Three patients experienced treatment-related deaths from pneumonia, liver failure and cerebral hemorrhage, respectively. It is concluded that Valspodar 10mg/kg per 24h in combination with daunorubicin 45mg/m2 for 3 days and cytarabine 1g/m2 twice daily for 4 days is tolerable in this heavily pre-treated group of patients. Due to the moderate treatment results, the phase II part of the study was ended prematurely. The modulation of only pgp did not give an obvious improvement of the treatment results in this group of patients. ⌐ 2002 Elsevier Science Ltd. All rights reserved.

  • 2.
    Knaust, Eva
    et al.
    Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet.
    Porwit-MacDonald, Anna
    Department of Pathology, Division of Hematology, Karolinska Hospital and Institutet, Stockholm, Sweden.
    Gruber, Astrid
    Departments of Medicine, Division of Hematology, Karolinska Hospital and Institutet, Stockholm, Sweden.
    Xu, Dawei
    Departments of Medicine, Division of Hematology, Karolinska Hospital and Institutet, Stockholm, Sweden.
    Peterson, Curt
    Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet.
    Different effects of metabolic inhibitors and cyclosporin A on daunorubicin transport in leukemia cells from patients with AML2003Ingår i: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 27, nr 2, s. 183-191Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The objective of this study was to determine the role of transport proteins in daunorubicin (Dnr) accumulation and efflux in leukemia cells from 36 patients with acute myeloid leukemia (AML). Mononuclear cells were isolated and incubated with 1 μM Dnr with/without addition of 3 μM cyclosporin A (CyA) or metabolic inhibitors (MI). Cellular Dnr concentration in leukemia blast cells was measured with flow cytometry. After washing and reincubation of the cells in drug-free medium, Dnr efflux was followed with/without addition of CyA or MI. Levels of mRNA expression for mdr1, multidrug resistance associated protein (mrp) and lung resistance protein (lrp) were determined with reverse transcriptase-polymerase chain reaction (RT-PCR). MI enhanced cellular Dnr accumulation to a higher extent than CyA whereas CyA reduced Dnr efflux more efficiently than MI (P<0.001). There was a significant difference in Dnr accumulation between samples with low and high mdr1 mRNA levels but only in the presence of MI or CyA. Our results imply that other factors than P-glycoprotein (Pgp) are of major importance for in vitro Dnr accumulation in AML blasts and that the role of Pgp as a drug efflux pump is not conclusive.

  • 3.
    Masquelier, Michéle
    et al.
    Karolinska, Stockholm.
    Lundgren, Bo
    Finland.
    Peterson, Curt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    Vitols, Sigurd
    Karolinska, Stockholm.
    Cytotoxic effect of a lipophilic alkylating agent after incorporation into low density lipoprotein or emulsions: Studies in human leukemic cells2006Ingår i: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 30, nr 2, s. 136-144Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The use of low density lipoprotein (LDL) as drug carrier in acute myeloblastic leukemia chemotherapy is attractive due to high LDL uptake by leukemic cells. Lipid-based formulations, such as liposomes or microemulsions are promising alternatives. In the current study, we incorporated N-trifluoroacetyl-adriamycin-14-valerate (AD32), a lipophilic derivative of daunorubicin (DNR), and WB4291, a lipophilic alkylating agent, into LDL or lipid microemulsions and evaluated their cytotoxic activities towards leukemic cell lines using as references DNR and melphalan. The incorporation of AD32 into LDL or emulsion resulted in complexes with poor cytotoxicity. WB4291-LDL and WB4291-emulsion exerted, on the other hand, promising cytotoxic effects towards parental and resistant K562 and HL60 cell lines. © 2005 Elsevier Ltd. All rights reserved.

  • 4.
    Norin, Stefan
    et al.
    Karolinska University Hospital, Sweden; Karolinska Institute, Sweden.
    Bjorkstrand, Bo
    Karolinska University Hospital, Sweden; Karolinska Institute, Sweden.
    Rommel, Franz
    Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Hematologiska kliniken US.
    Timberg, Lars
    Kristianstad Central Hospital, Sweden.
    Andersson, Per-Ola
    Sahlgrens University Hospital, Sweden.
    Haggstrom, Johan
    Kalmar Hospital, Sweden.
    Aldrin, Anders
    Visby Hospital, Sweden.
    Hansson, Lotta
    Karolinska University Hospital, Sweden; Karolinska Institute, Sweden.
    Severe infusion-related reactions are uncommon in rituximab-treated CLL patients in clinical practice: Results from a Swedish national observational study2015Ingår i: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 39, nr 1, s. 33-37Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    There have been concerns about serious infusion-related adverse drug reactions (ADR) with rituximabin chronic lymphocytic leukemia (CLL). We therefore conducted an observational trial in which CLL patients planned for rituximab-containing therapy were eligible. Ninety-six patients from 19 centers were enrolled. The most common regimen was rituximab, fludarabine and cyclophosphamide. Fifty-six patients experienced ADR during rituximab infusion. Reactions greater than= grade 3 occurred in five patients and no cases of tumor lysis syndrome were recorded. Despite a high number of circulating tumor cells few severe ADR were noted. Thus, rituximab containing regimens can be considered safe for CLL patients in general practice.

  • 5.
    Uggla, Bertil
    et al.
    Örebro University Hospital, Sweden .
    Ståhl, Elisabeth
    Örebro University Hospital, Sweden.
    Wågsäter, Dick
    Örebro University, Sweden.
    Paul, Christer
    Huddinge University Hospital, Stockholm, Sweden.
    Karlsson, Mats G.
    Örebro University Hospital, Sweden.
    Sirsjö, Allan
    Örebro University, Sweden.
    Tidefelt, Ulf
    Örebro University Hospital, Sweden .
    BCRP mRNA expression v. clinical outcome in 40 adult AML patients2005Ingår i: Leukemia research: a Forum for Studies on Leukemia and Normal Hemopoiesis, ISSN 0145-2126, E-ISSN 1873-5835, Vol. 29, nr 2, s. 141-146Artikel i tidskrift (Refereegranskat)
    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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