Group Pierre Åman

Research group
Active research
Project owner
The Institute of Biomedicine

Short description

Research on FET fusion oncoproteins and FET-SWI/SNF interactions.

Research summary

Chromosome rearrangements that lead to formation of fusion oncogenes have been identified in many types of leukemia and solid tumors. The FET-group of fusion oncogenes encode chimeric transcription factor proteins containing N-terminal parts of FET proteins juxtaposed to C-terminal DNA binding transcription factor parts.

Figure - research within the FET-SWI/SNF interactions

We have recently found that all FET-oncoproteins bind and change the activities of the SWI/SNF chromatin remodeling complex. Deregulation of SWI/SNF activity thus provides a unifying pathogenic mechanism for the large group of tumors caused by FET fusion oncoproteins.

Our research focus on the FET-SWI/SNF interactions and its consequences on molecular and cellular levels. Drug tests are also performed in vitro and in vivo and based on findings from our experimental systems.

Research tools and resources

Experimental systems: tumor cell lines, and xenograft models.

Methods: protein–protein interaction studies using recombinant proteins and immunoprecitpitation/mass spectometry. Chromatin immunoprecipitation (ChIP-seq), advanced microscopy, and single cell expression analysis.

Experimental findings are confirmed with studies on human tumor tissues.

Current group members

Pierre Åman, PhD, Professor
Mikael Kubista, Researcher
Christoffer Vannas, PhD student
Heba Albatrok, MSc, Associate Researcher

Selected publications

  1. FET family fusion oncoproteins target the SWI/SNF chromatin remodeling complex.
    Lindén M, Thomsen C, Grundevik P, Jonasson E, Andersson D, Runnberg R, Dolatabadi S, Vannas C, Luna Santamarίa M, Fagman H, Ståhlberg A, Åman P. EMBO Rep. (2019) Apr 8. pii: e45766. doi: 10.15252/embr.201845766.
  2. Phosphatidylinositol-3-kinase (PI3K)/Akt Signaling is Functionally Essential in Myxoid Liposarcoma.
    Trautmann M, Cyra M, Isfort I, Jeiler B, Kruger A, Grunewald I, Steinestel K, Altvater B, Rossig C, Hafner S, et al. (2019) Molecular cancer therapeutics, 10.1158/1535-7163.MCT-18-0763
  3. JAK-STAT signalling controls cancer stem cell properties including chemotherapy resistance in myxoid liposarcoma.
    Dolatabadi S, Jonasson E, Linden M, Fereydouni B, Backsten K, Nilsson M, Martner A, Forootan A, Fagman H, Landberg G, et al. (2019) Int J Cancer, 10.1002/ijc.32123
  4. Identification of inhibitors regulating cell proliferation and FUS-DDIT3 expression in myxoid liposarcoma using combined DNA, mRNA, and protein analyses.
    Svec D, Dolatabadi S, Thomsen C, Cordes N, Shannon M, Fitzpatrick P, Landberg G, Aman P, Stahlberg A (2018) Lab Invest 98: 957-967
  5. FUS-DDIT3 Fusion Protein-Driven IGF-IR Signaling is a Therapeutic Target in Myxoid Liposarcoma.
    Trautmann M, Menzel J, Bertling C, Cyra M, Isfort I, Steinestel K, Elges S, Grunewald I, Altvater B, Rossig C, et al. (2017) Clin Cancer Res 23: 6227-6238
  6. A new GTF2I-BRAF fusion mediating MAPK pathway activation in pilocytic astrocytoma.
    Tomic TT, Olausson J, Wilzen A, Sabel M, Truve K, Sjogren H, Dosa S, Tisell M, Lannering B, Enlund F, et al. (2017) PLoS One 12: e0175638
  7. Cell Cycle and Cell Size Dependent Gene Expression Reveals Distinct Subpopulations at Single-Cell Level.
    Dolatabadi S, Candia J, Akrap N, Vannas C, Tesan Tomic T, Losert W, Landberg G, Aman P, Stahlberg A (2017) Front Genet 8:1
  8. HSP90 inhibition blocks ERBB3 and RET phosphorylation in myxoid/round cell liposarcoma and causes massive cell death in vitro and in vivo.
    Safavi S, Jarnum S, Vannas C, Udhane S, Jonasson E, Tomic TT, Grundevik P, Fagman H, Hansson M, Kalender Z, et al. (2016) Oncotarget 7: 433-445
  9. Establishment and characterization of a new human myxoid liposarcoma cell line (DL-221) with the FUS-DDIT3 translocation.
    de Graaff MA, Yu JS, Beird HC, Ingram DR, Nguyen T, Juehui Liu J, Bolshakov S, Szuhai K, Aman P, Torres KE, et al. (2016) Lab Invest 96: 885-894
  10. HR23b expression is a potential predictive biomarker for HDAC inhibitor treatment in mesenchymal tumours and is associated with response to vorinostat.
    Angelika Ihle M, Merkelbach-Bruse S, Hartmann W, Bauer S, Ratner N, Sonobe H, Nishio J, Larsson O, Aman P, Pedeutour F, et al. (2016) J Pathol Clin Res 2: 59-71

More group Pierre Åman publications on PubMed


Pierre Åman
Photo: Emelie Asplund

Contact information

Pierre Åman

E-mail: Pierre Åman
Phone: +46 (0)31 786 6732

Visiting address:
Sahlgrenska Center
for Cancer Research,
Medicinaregatan 1F
413 90 Gothenburg

Navigate to video: FET oncogene sarcoma biology and drug development
Video (5:44)
FET oncogene sarcoma biology and drug development

Research presentation

Summary of ongoing research about novel interventions for patients diagnosed with FET sarcomas.

In collaboration with Professor Anders Ståhlberg.