Weischenfeldt Group

We are interested in the mutational mechanisms and clonal evolution of cancer, in particular mechanisms of complex structural variants and the impact on 3D chromatin organization. We are collaborating closely with clinicians, to identify the earliest mutational processes in a tumor.














Cancer is a disease of the genome, fueled by the accumulation of genomic alterations that improve the fitness of the cell. We use computational cancer genomics approaches to study clonal evolution and cancer stem cell models, with the overarching goal to understand the mutational processes that allow tumor cells to escape and evolve in time and space to cause treatment-resistance. We have a particular interest in the larger complex structural variants, their presence and impact on cancer stem cells and clonal evolution, and how they impact the chromatin architecture.

























Structural variant mediated chromatin alterations and enhancer hijacking mechanisms in cancer genomes

Evolutionary and mechanistic mutational forces shaping cancer genomes

Age-dependent mutational processes in cancer genomes










Clonal evolution analysis to identify recurrent mechanisms of treatment resistance and identify novel therapeutic targets

  • Predict clinical trajectories from cancer patients by developing methods to i) reconstruct and model the clonal evolution, ii) analyze clonal dynamics and interplay with tumor microenvironment. We are part of DANSTEM, with the overarching goal to study mechanisms of cancer stem cells.

Schematic of a clinical trajectory of a cancer patient (top), the clonal evolition (middle part) and mutational mechanisms (bottom). For detailed description please contact communication@bric.ku.dkHow complex structural variants emerge and affect the 3D chromatin architecture in cancer

  • Integrate epigenetic with somatic alterations and patient-related data using data-driven quantitative genetics-based computational approaches.
  • Apply chromatin architecture methodologies such as Hi-C to identify how genomic alterations can impact gene regulation through altered chromatin looping

SV-mediated Enhancer Hijacking. For further details and describtion of the figure please contact communication@bric.ku.dk



We use a combination of computational and molecular biology technologies to reach our research aims. We have optimized and integrated a range of different sequencing approaches on clinical material including paired-end sequencing, RNA-seq, ATAC-seq, Hi-C, Capture-Hi-C, mate-pair seq, DNA panel seq, single-cell sequencing, long-read sequencing. We carry out our compute on HPC systems, primarily computerome.dk. We use git for code version control and Docker to deploy our code on other systems.