Abstract
TP53 is probably the most extensively studied tumour-suppressor gene, and patients with TP53 mutations are known to have a poor outcome. However, inconsistencies in the analysis of TP53 status, and failure to realize that different mutations behave in different ways, prevent us from effectively applying our vast knowledge of this protein in clinical practice. What simple steps can be taken to ensure that patients benefit from our understanding of TP53?
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Amino Acid Substitution
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / physiology
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Gene Deletion
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Genes, Tumor Suppressor
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Genes, p53*
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Humans
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Li-Fraumeni Syndrome / genetics
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Li-Fraumeni Syndrome / mortality
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Loss of Heterozygosity
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Membrane Proteins*
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Mutation
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Mutation, Missense
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Neoplasms / genetics*
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Neoplasms / mortality
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Neoplasms / therapy
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Nuclear Proteins / genetics
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Nuclear Proteins / physiology
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Phosphoproteins / genetics
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Phosphoproteins / physiology
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Point Mutation
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Polymorphism, Genetic
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Prognosis
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RNA Splice Sites / genetics
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Structure-Activity Relationship
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Trans-Activators / genetics
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Trans-Activators / physiology
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Transcription Factors
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Transcriptional Activation
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Treatment Outcome
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Tumor Protein p73
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Tumor Suppressor Protein p53 / chemistry
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Tumor Suppressor Protein p53 / deficiency
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Proteins
Substances
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CKAP4 protein, human
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DNA-Binding Proteins
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Membrane Proteins
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Nuclear Proteins
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Phosphoproteins
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RNA Splice Sites
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TP63 protein, human
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Trans-Activators
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Transcription Factors
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Tumor Protein p73
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Tumor Suppressor Protein p53
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Tumor Suppressor Proteins