p53 and apoptosis

Research output: Contribution to journalArticlepeer-review

Abstract

Loss of function of the p53 tumour suppressor gene is a frequent and important event in the genesis or progression of many human malignancies. Loss of p53 dependent apoptosis is believed to be critical to carcinogenesis in many of these cases, suggesting the possibility to therapeutically restore this pathway and directly eliminate malignant cells or increase or restore their sensitivity to chemotherapeutic agents. The regulation of p53-dependent responses is complex and variable between cell types, and whether a cell undergoes apoptosis after activation of p53 is highly sensitive to signal context, including environmental and cell intrinsic influences. This article focuses upon p53-dependent apoptosis, considering current understanding of the biochemical steps involved, the factors determining selection of apoptosis over other p53-dependent responses, the significance of p53-dependent apoptosis for the genesis, progression and drug resistance of human cancers, and finally the prospects for clinical manipulation of this pathway in cancer therapy.
Original languageEnglish
Pages (from-to)522-38
Number of pages17
JournalBritish Medical Bulletin
Volume53
Issue number3
Publication statusPublished - 1997

Keywords

  • Apoptosis
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Cell Cycle
  • Cell Transformation, Neoplastic
  • DNA Damage
  • Genes, p53
  • Genetic Therapy
  • Humans
  • Mitogen-Activated Protein Kinases
  • Neoplasms
  • Oncogenes
  • Signal Transduction
  • Tumor Suppressor Protein p53
  • p38 Mitogen-Activated Protein Kinases

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