EMBO workshop

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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