Abstract

The p53 pathway has been shown to mediate cellular stress responses; p53 can initiate DNA repair, cell-cycle arrest, senescence and, importantly, apoptosis. These responses have been implicated in an individual's ability to suppress tumour formation and to respond to many types of cancer therapy. Here we focus on how best to use knowledge of this pathway to tailor current therapies and develop novel ones. Studies of the genetics of p53 pathway components — in particular p53 itself and its negative regulator MDM2 — in cancer cells has proven useful in the development of targeted therapies. Furthermore, inherited single nucleotide polymorphisms in p53 pathway genes could serve a similar purpose.

Author affiliations

1. Alexei Vazquez and Arnold J. Levine are at The Institute for Advanced Study, Einstein Drive, Princeton, New Jersey, 08540, USA.
2. Arnold J. Levine is at The Cancer Institute of New Jersey, 195 Little Albany Street, New Brunswick, New Jersey, 08903, USA.
3. Elisabeth E. Bond and Gareth L. Bond are at The Ludwig Institute of Cancer Research, University of Oxford, Old Road Campus, Oxford, OX3 7DQ, United Kingdom.

Correspondence to: Gareth L. Bond³ Email: gareth.bond@ndm.ox.ac.uk

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