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p53 as a target for anti-cancer drug development

Benjamin Pierre Bouchet1, Claude Caron de Fromentel, Alain Puisieux

  • 1INSERM U590, Centre Léon Bérard, 28 rue Laënnec, 69373 Lyon Cedex 08, France. bouchetb@lyon.fnclcc.fr

Critical Reviews in Oncology/Hematology
|May 13, 2006
PubMed

Insights

Restoring tumor suppressor p53 function is crucial for cancer therapy. Genetic and pharmacological strategies, including oncolytic viruses and small molecules, show promise in clinical trials for treating various cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Loss of p53 function impairs genetic stability and hinders cancer treatment efficacy.
  • Restoring p53 activity is a key goal in developing novel cancer therapies.

Purpose of the Study:

  • To review genetic and pharmacological strategies aimed at restoring or controlling p53 function in cancer patients.
  • To discuss the mechanisms and therapeutic perspectives of these p53-targeting approaches.

Main Methods:

  • Clinical evaluation of replication-deficient viruses carrying wild-type TP53 (Ad5CMV-p53) and oncolytic adenoviruses (ONYX-015).
  • Development of pharmacological agents, including small molecules (e.g., CP-31388, PRIMA-1), peptides (CDB3), and antibody fragments, to modulate p53 activity.
  • Analysis of synergistic effects between p53-based therapies and conventional chemotherapy.

Main Results:

  • Ad5CMV-p53 and ONYX-015 have shown clinical activity as monotherapy.
  • These viral strategies exhibit synergy with chemotherapy in certain cancer types.
  • Pharmacological agents are emerging to either stimulate wild-type p53 or restore function to mutant p53 proteins.

Conclusions:

  • Genetic and pharmacological interventions targeting p53 represent promising avenues for cancer treatment.
  • Further research into these approaches holds significant potential for improving patient outcomes in oncology.

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