Recurring chromosomal abnormalities have been identified in a variety of cancers and are frequently associated with hematological malignancies such as acute myeloid leukemia (AML). In addition to transcriptional activation of proto-oncogenes these cytogenetic changes often cause gene fusions leading to expression of chimeric oncofusion proteins. Our main research goal is to unravel the role of these oncofusion proteins in carcinogenesis. Our aim is to identify the binding regions, the transcriptional consequences and epigenetic features associated with oncofusion protein expression.
Next-generation sequencing and high-resolution transcription factor and epigenomic profiling are being used to identify oncofusion protein target sites which are subsequently characterized structurally as well as functionally in relation to the etiology of acute myeloid leukemia using both molecular as well as bioinformatic tools. These studies contribute to our understanding of both normal and aberrant hematopoietic development.