Kasper Fugger

Dr Kasper Fugger is Group Leader at the UCL Cancer Institute and leads a satellite lab at the Francis Crick Institute, where he has also been a Visiting Scientist since 2022. He earned his MSc and PhD degrees from the University of Copenhagen through studies at the Danish Cancer Institute, which focused on DNA replication, cell-cycle control, and genome stability. These studies established his long-standing interest in the mechanisms that protect the genome and prevent disease.

He continued this work during postdoctoral research in Copenhagen at the Biotech Research and Innovation Centre, where he further developed his expertise in genome maintenance and cancer biology. This foundation led him to pursue a second postdoctoral position at the newly established Francis Crick Institute, where he expanded his research towards nucleotide metabolism and its links to cancer therapy.

During his postdoctoral work at the Crick, Dr Fugger discovered that inhibition of the nucleotide detoxifying enzyme DNPH1 enhances the efficacy of PARP inhibitors and overcomes resistance in BRCA-deficient cancers. This finding opened a new translational direction in nucleotide metabolism, identified DNPH1 as a promising therapeutic target, and led to patents covering the use of DNPH1 inhibitors and hmdU nucleosides to sensitise homologous recombination-deficient cells to PARP inhibitor therapy. It also formed the basis for a collaboration with industry partners on a drug discovery programme to develop DNPH1 inhibitors, and this work was recognised by the 2021 Crick Scientific Award and by his appointment as a Crick Early Career Translation Fellow in 2022.

These discoveries helped establish his independent programme at UCL Cancer Institute, where his lab now investigates how pathological nucleotides arise, how they compromise genome integrity, and how cells detoxify them to prevent mutagenesis, tumour development, and neurological disease. The lab also studies the underlying mechanisms of these detoxification pathways and how their failure contributes to human disease. By combining functional genomics, cell biology, genetic screens, biochemistry, and chemical biology, his group studies nucleotide metabolism both as a fundamental mechanism of genome protection and as a source of therapeutic vulnerability. His research is supported by CRUK RadNet and Human Frontiers Science Program funding and is closely connected to collaborative and translational work across UCL and the Crick.