Stefán Þórarinn Sigurðsson

Stefan Sigurdsson received a BS degree in molecular biology from the University of Iceland in 1996 and a master's degree in molecular genetics from the same school in 1998. The focus of his studies was cancer biology, specifically the function of two tumor suppressor genes involved in breast cancer. He obtained his doctorate from the University of Texas 2003 where his research focused to DNA repair and DNA recombination. Stefan worked for five years as a postdoctoral fellow at Cancer Research UK where he studied transcription elongation by RNA polymerase II (RNAPII) and the connection between DNA damage and transcription elongation.

Genomic instability is a characteristic of most cancers, believed to arise because of the inability of cells to deal with damaged DNA. To prevent genomic instability, cells possess a complex network of processes collectively called the DNA damage response (DDR), which detects and repairs damaged DNA. This response is critical to prevent accumulation of mutations and DDR failure can lead to genomic instability and consequently cancer. Individuals with inherited DDR defects, such as mutations in ATM or BRCA2, are strongly associated with high cancer risk.

The overall aim of our work is to improve our understanding of how cancer develops and identify potential novel therapeutic targets. It is also of crucial importance in the clinic where cancer cells are treated with DNA damaging agents such as ionizing radiation and cytotoxic drugs. Increased knowledge on how the cell responds to such agents is a fundamental task in order to improve current cancer treatments.

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