Defying death after DNA damage

By T. Rich, R. Allen, A. Wyllie. Nature, 2000

802 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

DNA double-strand breaks: signaling, repair and the cancer connection (2001, background): “The G(2) checkpoint is maintained by redundant pathways.”
Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy (2006, background): “However, damage to DNA or to other critical molecules is considered to be a common initial event which is then propagated by the cellular stress response (Rich et al., 2000).”
On the origin, evolution, and nature of programmed cell death: a timeline of four billion years (2002, background): “Accordingly, genetic damage causes the activation of the p53 protein family, that induces either DNA repair and cell cycle arrest, or programmed cell death, a radical and extreme means preventing the emergence of genetic heterogeneity, and the progression towards cancer.(21)”
Mechanisms of human DNA repair: an update. (2003, background): “In higher eukaryotes a single non-repaired DSB inactivating an essential gene can be sufficient for inducing cell death via apoptosis (Rich et al., 2000).”
DNA damage and its links to neurodegeneration (2014, neutral): “Furthermore, even a few DSBs are sufficient to trigger apoptosis in proliferating cells (although whether neurons have a higher tolerance for DNA DSB accumulation has not been thoroughly investigated) (Rich et al., 2000).”
Chapter 1. General introduction (2015, positive): “Even a single unrepaired DSB may induce cell death (1).”