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Genome instability is a hallmark of human tumours and the underlining cause of several human syndromes. A central axis in the maintenance of genomic stability is the DNA damage response (DDR) – a complex signalling network that is activated most vigorously by critical DNA lesions such as double strand breaks (DSBs). The network spans DNA repair, damage tolerance pathways and cell cycle checkpoints, and modulates numerous processes impacting oncellular metabolism. It is not surprising, therefore, that several major players in the DDR are tumour suppressors, andthat germ-line mutations affecting DDR players lead to inherited predisposition to cancer, or more complex genomic instability syndromes including sporadic cancers.
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Prof. Vassilis G. Gorgoulis Laboratory of Histology-Embryology
Chair of Clinical Molecular Pathology, Ninewells Hospital and School of Medicine
University of Dundee, Dundee, UK
Biomedical Research Foundation of the Academy of Athens
Faculty Institute for Cancer Sciences, University of Manchester, Manchester Centre for Cellular Metabolism,
EMBO member
European Academy
Academia Europaea member
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