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  • 1.
    Gunnarsson, Niklas
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Leif, Stenke
    Hoglund, Martin
    Sandin, Fredrik
    Bjorkholm, Magnus
    Dreimane, Arta
    Lambe, Mats
    Markevärn, Berit
    Olsson-Stromberg, Ulla
    Richter, Johan
    Wadenvik, Hans
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Själander, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Second Malignancies Following Treatment of Chronic Myeloid Leukemia in the Tyrosine Kinase Inhibitor Era2014Ingår i: Blood, ISSN 0006-4971, E-ISSN 1528-0020, Vol. 124, nr 21Artikel i tidskrift (Övrigt vetenskapligt)
  • 2.
    Gunnarsson, Niklas
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Stenke, Leif
    Höglund, Martin
    Sandin, Fredrik
    Björkholm, Magnus
    Dreimane, Arta
    Lambe, Mats
    Markevärn, Berit
    Department of Haematology, University Hospital, Umeå.
    Olsson-Strömberg, Ulla
    Richter, Johan
    Wadenvik, Hans
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Själander, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Second malignancies following treatment of chronic myeloid leukaemia in the tyrosine kinase inhibitor era2015Ingår i: British Journal of Haematology, ISSN 0007-1048, E-ISSN 1365-2141, Vol. 169, nr 5, s. 683-688Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Given that tyrosine kinase inhibitors (TKIs) have dramatically improved the survival of patients with chronic myeloid leukaemia (CML), we were interested in examining the possible risk of long-term adverse events, such as the emergence of other neoplasms. Therefore, we studied the development of second malignancies in 868 patients diagnosed with CML between 2002 and 2011 using the Swedish CML register, cross-linked to the Swedish Cancer register. With a median follow-up of 3·7 (range 0-9·9) years, 65 (7·5%) patients developed 75 second malignancies (non-haematological), 52 of which were of the invasive type. Compared to expected rates in the background population, the risk of second malignancies was higher in the CML cohort, with a standardized incidence ratio (SIR) of 1·52 (95% CI 1·13-1·99). The SIR before and after the second year following diagnosis of CML was 1·58 and 1·47, respectively. Among specific cancer types, gastrointestinal and nose and throat cancer were significantly increased. Founded on a population-based material, our results indicate that CML patients treated in the TKI era are at an increased risk of developing a second malignancy, with indications that this risk may more likely be linked to CML itself rather than to the TKI treatment.

  • 3.
    Hayat, Amina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin. Internal Medicine Clinic, Sundsvall hospital, Sundsvall, Sweden.
    Själander, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin. Internal Medicine Clinic, Sundsvall hospital, Sundsvall, Sweden.
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin. Internal Medicine Clinic, Sundsvall hospital, Sundsvall, Sweden.
    Direct oral anticoagulants: patient reported adherence and minor bleedings2023Ingår i: Journal of Thrombosis and Thrombolysis, ISSN 0929-5305, E-ISSN 1573-742X, Vol. 56, nr 1, s. 55-64Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Data regarding adherence and minor bleeding on direct oral anticoagulants in everyday life are still sparse. Inclusion criteria: treatment initiated with dabigatran, rivaroxaban or apixaban in non-valvular atrial fibrillation patients from a center in northern Sweden between 2011 and 2019 (n = 668). Exclusion criteria: cognitive impairment, dose dispensing, need of interpreter or hospital admission (n = 67). By a telephone interview adherence was measured in 569 patients (response rate 94.8%) using the 8-item Morisky medication adherence scale and minor bleeding was asked for. CHA2DS2-VASc and HAS-BLED scores were collected from medical records. The number (n), mean age, mean treatment duration, mean (points) CHA2DS2-VASc and HAS-BLED scores was with dabigatran (n = 175, 73.3 years, 17.8 months, 3.6 p and 2.2 p), rivaroxaban (n = 198, 73.7 years, 21months, 3.8 p and 2.1 p) and apixaban (n = 196, 72.7 years, 15.2 months, 3.4 p and 2.1 p). Adherence was high for dabigatran, rivaroxaban and apixaban in 54%, 76% and 53%; intermediate in 37%, 20% and 37% or low in 9%, 4% and 10% respectively. High adherence (Morisky score 8) distinguished rivaroxaban (p < 0.0001) and in patients with CHA2DS2-VASc ≥ 4 p, (p < 0.0001). Patients on rivaroxaban/apixaban reported more minor bleedings (37% / 28%) compared to dabigatran (13%), (p < 0.001). Only 61% of the patients followed prescription. Adherence to rivaroxaban was significantly better, maybe due to the once daily dosing regimen, and furthermore among patients with higher risk for stroke. Minor bleedings were less common in the dabigatran group. The impact of minor bleedings on adherence and a possible relationship to clinical outcomes need to be further studied.

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  • 4.
    Malyukova, Alena
    et al.
    Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.
    Ujvari, Dorina
    Department of Women’s and Children’s Health, Karolinska Institute, Stockholm, Sweden.
    Yektaei-Karin, Elham
    Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.
    Zovko, Ana
    Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.
    Madapura, Harsha S.
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
    Keszei, Marton
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
    Nagy, Noemi
    Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
    Lotfi, Kourosh
    Department of Hematology, Linköping University Hospital, Linköping, Sweden; Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Björn, Niclas
    Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Tamai, Minori
    Department of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
    Nguyen, Thao T. T.
    Department of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
    Akahane, Koshi
    Department of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
    Inukai, Takeshi
    Department of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
    Stenke, Leif
    Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden; Division of Hematology, Karolinska University Hospital Solna, Stockholm, Sweden.
    Salamon, Daniel
    Department of Women’s and Children’s Health, Karolinska Institute, Stockholm, Sweden.
    Combination of tyrosine kinase inhibitors and the MCL1 inhibitor S63845 exerts synergistic antitumorigenic effects on CML cells2021Ingår i: Cell Death and Disease, ISSN 2041-4889, E-ISSN 2041-4889, Vol. 12, nr 10, artikel-id 875Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tyrosine kinase inhibitor (TKI) treatment has dramatically improved the survival of chronic myeloid leukemia (CML) patients, but measurable residual disease typically persists. To more effectively eradicate leukemia cells, simultaneous targeting of BCR-ABL1 and additional CML-related survival proteins has been proposed. Notably, several highly specific myeloid cell leukemia 1 (MCL1) inhibitors have recently entered clinical trials for various hematologic malignancies, although not for CML, reflecting the insensitivity of CML cell lines to single MCL1 inhibition. Here, we show that combining TKI (imatinib, nilotinib, dasatinib, or asciminib) treatment with the small-molecule MCL1 inhibitor S63845 exerted strong synergistic antiviability and proapoptotic effects on CML lines and CD34+ stem/progenitor cells isolated from untreated CML patients in chronic phase. Using wild-type BCR-ABL1-harboring CML lines and their T315I-mutated sublines (generated by CRISPR/Cas9-mediated homologous recombination), we prove that the synergistic proapoptotic effect of the drug combination depended on TKI-mediated BCR-ABL1 inhibition, but not on TKI-related off-target mechanisms. Moreover, we demonstrate that colony formation of CML but not normal hematopoietic stem/progenitor cells became markedly reduced upon combination treatment compared to imatinib monotherapy. Our results suggest that dual targeting of MCL1 and BCR-ABL1 activity may efficiently eradicate residual CML cells without affecting normal hematopoietic stem/progenitors.

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  • 5. Mulligan, Stephen P
    et al.
    Karlsson, Karin
    Strömberg, Mats
    Jønsson, Viggo
    Gill, Devinder
    Hammerström, Jens
    Hertzberg, Mark
    McLennan, Roger
    Uggla, Bertil
    Norman, John
    Wallvik, Jonas
    Sundström, Gunnel
    Johansson, Hemming
    Brandberg, Yvonne
    Liliemark, Jan
    Juliusson, Gunnar
    Cladribine prolongs progression-free survival and time to second treatment compared to fludarabine and high-dose chlorambucil in chronic lymphocytic leukemia2014Ingår i: Leukemia and Lymphoma, ISSN 1042-8194, E-ISSN 1029-2403, Vol. 55, nr 12, s. 2769-2777Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We conducted a randomized phase III trial to compare the efficacy and safety of two purine analogs, cladribine and fludarabine, with high-dose chlorambucil, in patients with previously untreated chronic lymphocytic leukemia (CLL). Between 1997 and 2004, 223 patients with CLL were randomly assigned to cladribine, fludarabine or chlorambucil, for six cycles of therapy with frequent health-related quality of life assessments. There was no statistical difference for the primary endpoint of overall response with cladribine (70%), fludarabine (67%) and chlorambucil (59%), or complete remission (12%, 7% and 8%), respectively. However, the median progression-free survival (25, 10, 9 months) and median time to second treatment (40, 22, 21 months) were superior with cladribine. There was no significant difference in overall survival (96, 82 and 91 months), nor in toxicity or HRQoL assessments. Monotherapy with cladribine gives superior PFS and longer response duration than fludarabine and chlorambucil as first-line treatment of CLL.

  • 6.
    Ujvari, Dorina
    et al.
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden; National Pandemic Center, Department of Microbiology, Tumor, and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Malyukova, Alena
    Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
    Zovko, Ana
    Division of Hematology, Karolinska University Hospital Solna, Stockholm, Sweden; Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Yektaei-Karin, Elham
    Division of Hematology, Karolinska University Hospital Solna, Stockholm, Sweden; Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Madapura, Harsha S.
    Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden.
    Keszei, Marton
    Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden.
    Nagy, Noemi
    Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
    Lotfi, Kourosh
    Department of Hematology, Linköping University Hospital, Linköping, Sweden; Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    Björn, Niclas
    Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Stenke, Leif
    Division of Hematology, Karolinska University Hospital Solna, Stockholm, Sweden; Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Salamon, Daniel
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    IFNγ directly counteracts imatinib-induced apoptosis of primary human CD34+ CML stem/progenitor cells potentially through the upregulation of multiple key survival factors2022Ingår i: Oncoimmunology, ISSN 2162-4011, E-ISSN 2162-402X, Vol. 11, nr 1, artikel-id 2109861Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tyrosine kinase inhibitors (TKIs) have dramatically improved the survival in chronic myeloid leukemia (CML), but residual disease typically persists even after prolonged treatment. Several lines of evidence suggest that TKIs administered to CML patients upregulate interferon γ (IFNγ) production, which may counteract the anti-tumorigenic effects of the therapy. We now show that activated T cell-conditioned medium (TCM) enhanced proliferation and counteracted imatinib-induced apoptosis of CML cells, and addition of a neutralizing anti-IFNγ antibody at least partially inhibited the anti-apoptotic effect. Likewise, recombinant IFNγ also reduced imatinib-induced apoptosis of CML cells. This anti-apoptotic effect of IFNγ was independent of alternative IFNγ signaling pathways, but could be notably diminished by STAT1-knockdown. Furthermore, IFNγ upregulated the expression of several anti-apoptotic proteins, including MCL1, PARP9, and PARP14, both in untreated and imatinib-treated primary human CD34+ CML stem/progenitor cells. Our results suggest that activated T cells in imatinib-treated CML patients can directly rescue CML cells from imatinib-induced apoptosis at least partially through the secretion of IFNγ, which exerts a rapid, STAT1-dependent anti-apoptotic effect potentially through the simultaneous upregulation of several key hematopoietic survival factors. These mechanisms may have a major clinical impact, when targeting residual leukemic stem/progenitor cells in CML.

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  • 7. 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)
  • 8. Yektaei-Karin, E.
    et al.
    Zovko, A.
    Nilsson, A.
    Kanter, L.
    Radmark, O.
    Ekblom, M.
    Qian, H.
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Stenke, L.
    MODULATION OF LEUKOTRIENE SIGNALING INHIBITING CELL GROWTH IN CHRONIC MYELOID LEUKEMIA2016Ingår i: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 101, s. 731-731Artikel i tidskrift (Övrigt vetenskapligt)
  • 9. 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.

  • 10. Zovko, Ana
    et al.
    Yektaei-Karin, Elham
    Salamon, Daniel
    Nilsson, Anders
    Wallvik, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Stenke, Leif
    Montelukast, a cysteinyl leukotriene receptor antagonist, inhibits the growth of chronic myeloid leukemia cells through apoptosis2018Ingår i: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 40, nr 2, s. 902-908Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The clinical outcome for patients with chronic myeloid leukemia (CML) has improved significantly with the introduction of tyrosine kinase inhibitors (TKIs). However, their curative potential appears limited, probably as a consequence of TKI-resistant leukemic stem cells (LSCs) that persist as a result of aberrant pathways independent of the well-established oncoprotein Bcr-Abl. One such pathway involves signaling through leukotrienes (LTs), bioactive compounds that have been suggested to play a role in several other malignancies. Cysteinyl LT1 receptor (CysLT1R) has been reported to be overexpressed in a number of solid cancers, and blocking of this receptor with the antagonist montelukast (treatment approved for bronchial asthma) has resulted in the killing of cancer cells. We recently demonstrated that montelukast, alone or in combination with imatinib, can effectively reduce the growth of CML cells, while normal bone marrow cells were left unaffected. Herein, we further investigated the importance of CysLT1R for the survival of CML cells and the mechanisms by which montelukast induces cell death. Knockdown of the CysLT1R of K562 cells with siRNA reduced their growth by 25%. Montelukast had no effect on these cells, while it killed more than 50% of CysLT1R-expressing cells. Growth inhibition exerted by imatinib was unaffected by CysLT1R status. Montelukast-induced killing of K562/JURL-MK1 CML cells was paralleled by Bax overexpression, cytochrome c release, PARP-1 cleavage, and caspase-3 activation, an event further increased in a setting where montelukast was added to imatinib. Wnt/-catenin signaling was activated by CysLT1R and we observed that montelukast could induce proteins in this pathway, a finding of relevance for LSC survival. Thus, montelukast, employed at in vivo-like concentrations, induces the killing of CML cells through apoptotic pathways and may provide an additional, novel therapeutic possibility in CML.

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