Small molecules that reactivate mutant p53

Eur J Cancer. 2003 Sep;39(13):1828-34. doi: 10.1016/s0959-8049(03)00454-4.

Abstract

Around half of all human tumours carry mutant p53. This allows escape from p53-induced cell cycle arrest and apoptosis. Many tumours express mutant p53 proteins at elevated levels. Restoration of wild-type p53 function should trigger massive apoptosis in tumour cells and thus eradicate tumours. Various types of small molecules have been identified that can restore native conformation and wild-type function to mutant p53. Such molecules may serve as leads for the development of novel efficient anticancer drugs.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antineoplastic Agents, Phytogenic / therapeutic use
  • Apoptosis / genetics
  • Aza Compounds / therapeutic use
  • Bridged Bicyclo Compounds, Heterocyclic / therapeutic use
  • Ellipticines / therapeutic use
  • Gene Expression Regulation, Neoplastic*
  • Genes, p53 / genetics*
  • Genetic Therapy / methods
  • Humans
  • Mercaptoethylamines / therapeutic use
  • Molecular Chaperones / physiology
  • Mutation / genetics*
  • Neoplasms / genetics*
  • Neoplasms / pathology
  • Neoplasms / therapy
  • Pyrimidines / therapeutic use

Substances

  • Antineoplastic Agents, Phytogenic
  • Aza Compounds
  • Bridged Bicyclo Compounds, Heterocyclic
  • Ellipticines
  • Mercaptoethylamines
  • Molecular Chaperones
  • Pyrimidines
  • N-(2-mercaptoethyl)-1,3-diaminopropane
  • 2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one
  • CP 31398