Welcome to the Radiation Biology and DNA Damage Signaling group.
Our goal is to obtain new knowledge about the molecular mechanisms of DNA damage-induced signaling pathways, and to explore potential clinical applications of such knowledge.
In response to DNA damage, human cells activate signaling cascades that control cellular processes such as DNA damage repair, cell cycle checkpoint arrest, and induction of cell death. Over the past years intensive research in many laboratories have revealed several such signal cascades in some molecular detail. However, several major issues remain unresolved, both with respect to understanding the molecular mechanisms, and to understanding how this new knowledge about DNA damage signaling cascades can be applied to improve cancer therapy.
In response to DNA damage, human cells activate signaling cascades that control cellular processes such as DNA damage repair, cell cycle checkpoint arrest, and induction of cell death. Over the past years intensive research in many laboratories have revealed several such signal cascades in some molecular detail. However, several major issues remain unresolved, both with respect to understanding the molecular mechanisms, and to understanding how this new knowledge about DNA damage signaling cascades can be applied to improve cancer therapy.

News & events
Understanding breast cancer
Landscape of cancer genes and mutational processes in breast cancer
May 21, 2012
More news
Landscape of cancer genes and mutational processes in breast cancer
May 21, 2012
Latest publications
Randi Syljuåsen's group
Safeguarding genome integrity: the checkpoint kinases ATR, CHK1 and WEE1 restrain CDK activity during normal DNA replication
Nucleic Acids Res, 40 (2), 477-86
PubMed 21937510
The amount of DNA damage needed to activate the radiation-induced G2 checkpoint varies between single cells
Radiother Oncol, 101 (1), 24-7
PubMed 21722983
A genetic screen identifies BRCA2 and PALB2 as key regulators of G2 checkpoint maintenance
EMBO Rep, 12 (7), 705-12
PubMed 21637299
More publications




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