Abstract

DNA damage responses (DDR) encompass DNA repair and signal transduction pathways that effect cell cycle checkpoint arrest and/or apoptosis. How DDR pathways respond to low levels of DNA damage, including low doses of ionizing radiation, is crucial for assessing environmental cancer risk. It has been assumed that damage-induced cell cycle checkpoints respond to a single double strand break (DSB) but the G2/M checkpoint, which prevents entry into mitosis, has recently been shown to have a defined threshold of 10–20 DSBs. Here, we consider the impact of a negligent G2/M checkpoint on genomic stability and cancer risk.

Author affiliations

1. Markus Löbrich is at the Darmstadt University of Technology, Radiation Biology and DNA Repair, 64287 Darmstadt, Germany.
2. Penny A. Jeggo is at the Genome Damage and Stability Centre, University of Sussex, East Sussex, BN1 9RQ, UK.

Correspondence to: Markus Löbrich¹ Email: lobrich@bio.tu-darmstadt.de

Correspondence to: Penny A. Jeggo¹ Email: p.a.jeggo@sussex.ac.uk

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