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
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antineoplastic Agents, Phytogenic / therapeutic use
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Apoptosis / genetics
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Aza Compounds / therapeutic use
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Bridged Bicyclo Compounds, Heterocyclic / therapeutic use
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Ellipticines / therapeutic use
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Gene Expression Regulation, Neoplastic*
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Genes, p53 / genetics*
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Genetic Therapy / methods
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Humans
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Mercaptoethylamines / therapeutic use
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Molecular Chaperones / physiology
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Mutation / genetics*
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Neoplasms / genetics*
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Neoplasms / pathology
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Neoplasms / therapy
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Pyrimidines / therapeutic use
Substances
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Antineoplastic Agents, Phytogenic
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Aza Compounds
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Bridged Bicyclo Compounds, Heterocyclic
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Ellipticines
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Mercaptoethylamines
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Molecular Chaperones
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Pyrimidines
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N-(2-mercaptoethyl)-1,3-diaminopropane
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2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one
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CP 31398