Abstract
The response of cells to DNA damage is critical for maintaining genomic integrity and for preventing cancer development. Current advances in our understanding of the response of cells to DNA double-strand breaks and to stalled DNA replication forks and the relationship of these responses to human disease were discussed at the 52nd Benzon Symposium in Denmark, Copenhagen. Here we review the novel findings that were presented at this Symposium and the current state of the field.
MeSH terms
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle Proteins / metabolism
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Checkpoint Kinase 1
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Chromatin / genetics
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Chromatin / metabolism
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DNA Damage*
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DNA Repair / genetics
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DNA Repair / physiology
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DNA Replication
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DNA-Binding Proteins / metabolism
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Denmark
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Genetic Diseases, Inborn / genetics
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Genetic Diseases, Inborn / metabolism
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Humans
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Models, Biological
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Neoplasms / genetics
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Neoplasms / metabolism
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Protein Kinases / metabolism
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Protein Serine-Threonine Kinases / metabolism
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Telomere / genetics
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Telomere / metabolism
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Translocation, Genetic
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Tumor Suppressor Protein p53 / metabolism
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Tumor Suppressor Proteins / metabolism
Substances
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Cell Cycle Proteins
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Chromatin
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DNA-Binding Proteins
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Tumor Suppressor Protein p53
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Tumor Suppressor Proteins
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Protein Kinases
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ATM protein, human
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ATR protein, human
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Ataxia Telangiectasia Mutated Proteins
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Checkpoint Kinase 1
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Protein Serine-Threonine Kinases