¹Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, Epalinges CH-1066, Switzerland

Correspondence: J Tschopp, Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, Epalinges CH-1066, Switzerland. Tel: +41 21 6925738; Fax: +41 21 6925705; E-mail: jurg.tschopp@unil.ch

Received 13 October 2005; Revised 10 November 2005; Accepted 15 November 2005; Published online 13 January 2006.

Abstract

An appropriate response to genotoxic stress is essential for maintenance of genome stability and avoiding the passage to neoplasia. Nuclear factor B (NF-B) is activated as part of the DNA damage response and is thought to orchestrate a cell survival pathway, which, together with the activation of cell cycle checkpoints and DNA repair, allows the cell in cases of limited damage to restore a normal life cycle, unharmed. In this respect, NF-B is one of the main factors accounting for chemotherapy resistance and as such impedes effective cancer treatment, representing an important drug target. Despite this high clinical relevance, signalling cascades leading to DNA damage-induced NF-B activation are poorly understood and the use of highly divergent experimental set-ups in the past led to many controversies in the field. Therefore, in this review, we will try to summarize the current knowledge of distinct DNA damage-induced NF-B signalling pathways.