Till startsida
University of Gothenburg
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Group Pierre Åman

Research summary

Chromosome rearrangements that lead to formation of fusion genes have been identified in many types of leukemia and solid tumors. Around 700 different fusion oncogenes are currently reported in human neoplasias. Many of them were found to transform cells in culture and to induce tumors in transgenic mice, showing their importance in tumor development. Many fusion genes are associated with only one type of tumors. The tumor type specificity suggests that their products interact with distinct differentiation controlling gene programs and cell types.

The aim of our research is to investigate the activities of the FET group of fusion oncogenes. They all encode chimeric transcription factor proteins containing a C-terminal DNA binding transcription factor part juxtaposed to an ectopic N-terminal protein interacting part. The FET oncogenes are strictly tumor type specific.

We have developed experimental systems to study the abnormal transcription factor activity and downstream effects of FET-oncogenes. We hope to increase our understanding of how their activities lead to tumor formation and how they interact with growth and differentiation controlling gene programs in different cell types. Many observations suggest that tumor development is initiated in stem or precursor cells and our current research focus on such cells.

Our main experimental activities focus on the myxoid liposarcoma/round cell sarcoma specific FUS-CHOP and the Ewing sarcoma EWS-FLI1 fusion oncogenes and the interaction of their protein products with the control of cell growth, differentiation, stress, stemness and senescence.

Research tools and resources

Experimental systems: tumor cell lines, stemcell, and xenograft models.

Methods: single cell expression analysis, advanced microscopy, and protein–protein interaction studies using recombinant proteins.

Experimental findings are confirmed with studies on human tumor tissues.

Current group members

Pierre Åman, PhD, Professor
Ayman Osman, PhD, Post doc
Christoffer Vannas, PhD student
Malin Lindén, PhD student

Selected publications

  1. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. Regulatory mechanisms, expression levels and proliferation effects of the FUS-DDIT3 fusion oncogene in liposarcoma.
    Aman P, Dolatabadi S, Svec D, Jonasson E, Safavi S, Andersson D, Grundevik P, Thomsen C, Stahlberg A (2016) J Pathol 238: 689-699


More group Pierre Åman publications on PubMed

Contact information

Pierre Åman

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

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


Page Manager: Yael Zukovsky Fitoussi|Last update: 3/21/2019

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