Cancer is a genetic disease and is caused by accumulation of genomic alterations that improve the fitness of the cell. We utilize cancer genomics approaches to characterize the mechanisms, functional consequences and prognostic relevance of genomic alterations in cancer.
We combine computational and molecular biology approaches to study genotype-phenotype associations in cancer. The main areas of research involve clonal evolution reconstruction in cancer to identify mechanisms of disease progression and to identify the mechanisms and functional consequences of large structural variants in cancer genomes. We are collaborating with clinicians to identify novel biomarkers and to stratify patients based on mutational profiles. A long-term goal is to provide personalized therapeutic intervention options for clinical decision-making.
- Develop and apply a novel algorithm to reconstruct the molecular evolution and identify disease trajectories from sequencing data (Gerhäuser et al, Cancer Cell, 2018)
- Identify the earliest mutational processes in prostate cancer (Gerhäuser et al, Cancer Cell, 2018)
- Characterize novel mechanisms of SV-mediated oncogene activation known as enhancer hijacking (Northcott et al, Nature, 2017, Weischenfeldt et al. Nat Genet, 2016)
- Identify link between germline predisposing variants and massive somatic genomic alterations (chromothripsis) (Rausch et al, Cell, 2012; Mardin et al, Mol Syst Biol, 2015)
- Discovery of age-related genomic alteration mechanism in prostate cancer (Weischenfeldt et al, Cancer Cell, 2013)
Joachim Weischenfeldt obtained his PhD from University of Copenhagen. Following a post doc at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, he started as a group leader at the Finsen Laboratory in September 2015.
Our work is funded by:
- Danish Council for Independent Research
- Arvid Nilssons fond
- Novo Nordisk Foundation
- Danish Cancer Society
- National Institute of Health (NIH), US