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