Welcome to Stig Ove Bøe's research group:

Experimental Cancer Therapy

 
S. O. Bøe
S. O. Bøe

Acute promyelocytic leukemia (APL) is a subtype of acute myelogenous leukemia (APL) 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
click to enlarge image

 

 
 

Selected publications

 
  1. 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

  2. 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

  3. 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

  4. 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

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

  6. 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

  7. 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

  8. 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

  9. 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
 
 

Contact information

 

Email: stig.ove.boe@rr-research.no; Phone +47 23070947