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The tumour suppressor activity of p53 plays a major role in limiting abnormal proliferation, and inactivation of the p53 response is becoming increasingly accepted as a hallmark of cancer. In contrast, both p63 and p73, which are close relatives of p53, are rarely mutated in tumour cells. At a theoretical level, therapeutic approaches that reinstate p53 activity, or augment p63 and p73, provide plausible and potentially efficacious routes towards new cancer treatments. Equally important is the clinical need to increase the efficacy of conventional anti-cancer drugs. Incapacitating the p53 response to limit the side effects in healthy cells may be one approach towards increasing the therapeutic window of many current anti-cancer drugs. Nevertheless, while cancer drug discovery focussed on p53 is an exciting and realistic possibility, translating this concept into a clinical setting is likely to be challenging.

Type

Journal article

Journal

Prog Cell Cycle Res

Publication Date

2003

Volume

5

Pages

375 - 382

Keywords

Animals, Antineoplastic Agents, Cell Division, DNA-Binding Proteins, Drug Design, Genes, Tumor Suppressor, Humans, Membrane Proteins, Molecular Structure, Neoplasms, Nuclear Proteins, Phosphoproteins, Trans-Activators, Transcription Factors, Tumor Protein p73, Tumor Suppressor Protein p53, Tumor Suppressor Proteins