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Functional Tumor GenomicsTumorgenomik

Functional Tumor Genomics

Our group is interested in the interplay between functional genomic elements and epigenetic features and how their interactions shape cellular identity. Disruption of the genomic context these interactions take place in can cause deregulation of the associated transcriptional programs thereby fueling cellular transformation, as happening in several hematopoietic cancers by translocations between highly active immunoglobulin genes and growth control loci. Given the fact that the human genome contains more regulatory than coding regions, additional non-coding aberrations presumably influence cellular growth control pathways and thereby change cellular fate.

Therefore, our research focuses on the characterization of regulatory sites and their interactions with transcription factors and epigenetic modifiers. Understanding how pivotal regulatory circuits are maintained and how oncogenic driver events are generated by their disruption is a central goal of our work. Moreover, we explore the molecular consequences of deregulated genes as well as the mechanisms preserving epigenetic information.

Combining NGS-based methods with bioinformatic approaches, we aim to unravel the consequences of regulatory mutations, how they reshape the epigenetic landscape and alter transcriptional networks. Besides examining these effects in model systems closely resembling genomic aberrations found in cancer patients, we deploy genome editing to reconstruct particular events and follow their molecular effects.

Furthermore, by performing targeted RNA-sequencing we advance the characterization of the cell lines in our collection. In order to provide data-based guidelines for the selection of ideal model lines for individual types of cancer containing recurrent aberrations, we screen for a multitude of cancer-relevant genes, their expression and their mutational status as well as for putative gene-fusions.

Photo of Max  Koeppel
Dr. Koeppel, Max
Phone: +49-531/2616-164


Javierre B.M. et al.: Lineage-specific genome architecture links enhancers and non-coding disease variants to target gene promoters. Cell. 2016; 167(5):1369-1384.

Puente X.S. et al.: Non-coding recurrent mutations in chronic lymphocytic leukaemia. Nature. 2015; 526(7574):519-24.

Ernst J., Kellis M. ChromHMM: automating chromatin-state discovery and characterization. Nat Methods. 2012; 9(3):215-6.