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Achilles' heel of cancer?

Nature volume 412, pages 865–866 (2001)Cite this article

The p53 protein is inactivated in most human cancers. One outcome is a defect in controlling cell division. Might a virus that exploits this defect prove useful in treating cancer?

A decade or so ago, it was discovered that the p53 protein is subtly mutated, and thereby inactivated, in almost all types of human cancer1,2. These findings raised the exciting possibility that drugs that restore p53's function would be broadly applicable cancer treatments. That hope has not yet been realized, but there have been some imaginative approaches to the problem — the latest of which is described by Raj and colleagues on page 914 of this issue3.

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Figure 1: The strategy used by Raj et al.3 to kill cells that lack p53.

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Authors and Affiliations

  1. Howard Hughes Medical Institute and Johns Hopkins Oncology Center, Baltimore, 21231, Maryland, USA

    Bert Vogelstein & Kenneth W. Kinzler

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  1. Bert Vogelstein
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  2. Kenneth W. Kinzler
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Vogelstein, B., Kinzler, K. Achilles' heel of cancer?. Nature 412, 865–866 (2001). https://doi.org/10.1038/35091170

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