Abstract
Numerous parameters influenced tumour radiosensitivity. The number of clonogenic cells, growth fraction, hypoxia and intrinsic radiosensitivity are among the most important determinants of radiocurability. Detection of DNA damage and repair pathways are important components of intrinsic radiosensitivity. ATM plays a major role in the cellular response to ionizing radiation: it induced DNA repair, cell cycle arrest, and apoptosis via induction of p53. Analysis of single nucleotide polymorphisms could help us to predict normal tissue sensitivity on an individual basis. Mutations of ATM is probably involved in some cases of severe radiation-induced late effects. Measure of residual double-strand breaks by immunochemistry of H2AX, but also ATM or MRE11, is another way to evaluate tumour radiosensitivity. Integration of genomics and functional approach are needed to better predict what the best candidates for a curative radiotherapy are.
MeSH terms
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Apoptosis
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle / physiology
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Cell Cycle Proteins / analysis
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Cell Cycle Proteins / genetics*
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Cell Cycle Proteins / physiology
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DNA Damage*
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DNA Repair / physiology*
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DNA-Binding Proteins / analysis
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DNA-Binding Proteins / genetics*
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DNA-Binding Proteins / physiology
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Histones / analysis
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Humans
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MRE11 Homologue Protein
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Mutation / physiology
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Neoplasms / genetics
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Neoplasms / radiotherapy*
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Protein Serine-Threonine Kinases / analysis
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Protein Serine-Threonine Kinases / genetics*
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Protein Serine-Threonine Kinases / physiology
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Radiation Injuries / genetics
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Radiation Tolerance / genetics*
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Tumor Suppressor Proteins / analysis
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Tumor Suppressor Proteins / genetics*
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Tumor Suppressor Proteins / physiology
Substances
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Cell Cycle Proteins
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DNA-Binding Proteins
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H2AX protein, human
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Histones
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MRE11 protein, human
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Tumor Suppressor Proteins
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ATM protein, human
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Ataxia Telangiectasia Mutated Proteins
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Protein Serine-Threonine Kinases
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MRE11 Homologue Protein