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Nature 443, 153-154 (14 September 2006) | doi:10.1038/443153a; Published online 13 September 2006

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Cancer biology: Can less be more for p53?

Anton Berns1

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The tumour-suppressor protein p53 is often mutated in cancer. But it seems that p53 deficiency is not all bad, and inhibiting this protein might mitigate toxic side effects of chemotherapy and radiotherapy.

The p53 protein gained its reputation as the 'guardian of the genome' because it mediates the cell's response to certain types of injury, relaying signals from both the DNA-damage response pathway and the oncogenic (tumour-promoting) stress pathway. Defects in these pathways are associated with a predisposition to cancer, and because they converge on p53, it has always been assumed that they act primarily through this crucial protein.

  1. Anton Berns is in the Division of Molecular Genetics and Centre of Biomedical Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
    Email: a.berns@nki.nl

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