Abstract
DNA damage responses (DDR) encompass DNA repair and signal transduction pathways that effect cell cycle checkpoint arrest and/or apoptosis. How DDR pathways respond to low levels of DNA damage, including low doses of ionizing radiation, is crucial for assessing environmental cancer risk. It has been assumed that damage-induced cell cycle checkpoints respond to a single double strand break (DSB) but the G2/M checkpoint, which prevents entry into mitosis, has recently been shown to have a defined threshold of 10-20 DSBs. Here, we consider the impact of a negligent G2/M checkpoint on genomic stability and cancer risk.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Apoptosis / physiology
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / physiology*
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Cell Division / physiology*
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / pathology*
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DNA / radiation effects
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DNA Breaks, Double-Stranded
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DNA Damage*
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DNA Repair / physiology*
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / physiology*
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G2 Phase / physiology*
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Genes, cdc
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Genomic Instability*
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Humans
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Intracellular Signaling Peptides and Proteins / physiology
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Models, Biological
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Phosphorylation
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Protein Processing, Post-Translational
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / physiology*
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Risk
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Signal Transduction / genetics
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Signal Transduction / physiology
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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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Intracellular Signaling Peptides and Proteins
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Tumor Suppressor Proteins
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DNA
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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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Protein Serine-Threonine Kinases