Welcome to Stig Ove Bøe's research group: Experimental Cancer Therapy

S. O. BøeGroup leader
S. O. Bøe
Group leader

Acute promyelocytic leukemia (APL) is a subtype of acute myelogenous leukemia (AML) that arises due to a block in blood cell development at the promyelocytic stage of differentiation. APL is characterized by a t(15;17) chromosomal translocation that fuses the gene encoding promyelocytic leukemia protein (PML) to that encoding retinoic acid receptor alpha (RARA). The product of this genetic aberration, the PML/RARA fusion protein, is an oncoprotein and represents one of the major contributing factors for APL development.

Research during the past 20 years have led to the discovery of two reagents, al trans retinoic acid (ATRA) and arsenic trioxide (ATO), that cure APL through a mechanism that involves direct targeting of the PML/RARA oncoprotein. Since APL is caused by a defined genetic alteration (the t(15;17) translocation) and because of the success of treating this disease by targeted therapeutic drugs, APL has become one of the most attractive model diseases for the development of targeted cancer therapy.

In our work we attempt to elucidate the molecular mechanisms involved in development and treatment of APL. Our goal is to identify therapeutic concepts that can be generalized and applied for treatment of other cancers. To achieve this we use a wide range of molecular biology and cell biology techniques, including live cell imaging, mass spectrometry and flow cytometry. We also use mouse models for in vivo experiments and we collaborate with clinicians to study primary tumor samples.

PML bodies

Selected publications

  1. Lång A, Lång E, Bøe SO.
    PML Bodies in Mitosis.
    Cells. 2019 Aug 14;8(8). pii: E893. doi: 10.3390/cells8080893. Review.
    PMID: 31416160

  2. Lång E, Polec A, Lång A, Valk M, Blicher P, Rowe AD, Jackson C, Utheim TP, Janssen LMC, Eriksson JE, Bøe SO
    Coordinated collective migration and asymmetric cell division in confluent human keratinocytes without wounding
    Nat Commun. 9 (1), 3665 DOI 10.1038/s41467-018-05578-7,
    PMID 30202009

  3. Lång A, Øye A, Eriksson J, Rowe AD, Lång E, Bøe SO.
    Influence of acute promyelocytic leukemia therapeutic drugs on nuclear pore complex density and integrity.
    Biochem Biophys Res Commun. 2018 May 15;499(3):570-576.
    PMID: 29596829

  4. Lång A, Eriksson J, Schink KO, Lång E, Blicher P, Połeć A, Brech A, Dalhus B, Bøe SO.
    Visualization of PML nuclear import complexes reveals FG-repeat nucleoporins at cargo retrieval sites.
    Nucleus. 2017 Apr 12:1-17.
    PMID: 28402725

  5. Palibrk V, Suganthan R, Scheffler K, Wang W, Bjørås M, Bøe SO (2016)
    PML regulates neuroprotective innate immunity and neuroblast commitment in a hypoxic-ischemic encephalopathy model
    Cell Death Dis, 7 (7), e2320
    PubMed 27468695
  6. Palibrk V, Lång E, Lång A, Schink KO, Rowe AD, Bøe SO (2014)
    Promyelocytic leukemia bodies tether to early endosomes during mitosis
    Cell Cycle, 13 (11), 1749-55
    PubMed 24675887

  7. Lång E, Grudic A, Pankiv S,Bruserud O, Simonsen A,Bjerkvig R, Bjørås M, Bøe SO
    The arsenic-based cure of acute promyelocytic leukemia promotes cytoplasmic sequestration of PML and PML/RARA through inhibition of PML body recycling
    Blood. 2012 Jul 26;120(4):847-57. 
    PubMed 22692509

  8. Jul-Larsen A, Grudic A, Bjerkvig R, Bøe SO (2010)
    Subcellular distribution of nuclear import-defective isoforms of the promyelocytic leukemia protein
    BMC Mol Biol, 11, 89
    PubMed 21092142

  9. Bøe SO, Simonsen A (2010)
    Autophagic degradation of an oncoprotein
    Autophagy, 6 (7), 964-5
    PubMed 20724820

  10. Isakson P, Bjørås M, Bøe SO, Simonsen A (2010)
    Autophagy contributes to therapy-induced degradation of the PML/RARA oncoprotein
    Blood, 116 (13), 2324-31
    PubMed 20574048

  11. Jul-Larsen A, Grudic A, Bjerkvig R, Bøe SO (2009)
    Cell-cycle regulation and dynamics of cytoplasmic compartments containing the promyelocytic leukemia protein and nucleoporins
    J Cell Sci, 122 (Pt 8), 1201-10
    PubMed 19339552

  12. Grudic A, Jul-Larsen A, Haring SJ, Wold MS, Lønning PE, Bjerkvig R, Bøe SO (2007)
    Replication protein A prevents accumulation of single-stranded telomeric DNA in cells that use alternative lengthening of telomeres
    Nucleic Acids Res, 35 (21), 7267-78
    PubMed 17959650

  13. Bøe SO, Haave M, Jul-Larsen A, Grudic A, Bjerkvig R, Lønning PE (2006)
    Promyelocytic leukemia nuclear bodies are predetermined processing sites for damaged DNA
    J Cell Sci, 119 (Pt 16), 3284-95
    PubMed 16868026