Abstract
Integrity of genome is a prerequisite for cell viability. Therefore, targeted damage of DNA structure is considered the key approach to the induction of cell death. Among the plethora of death execution programs the mitochondrial events are of the utmost importance. However, the epigemetic activation of defense mechanisms in response to DNA damage limit cell death. This review analyses the outcome of the genotoxic stress (i.e., cell death versus survival) as a balance of pro- and anti-apoptotic signaling. Practically speaking, the combinations of DNA damaging agents with the inhibitors of anti-apoptosis would increase the efficacy of anticancer therapy.
MeSH terms
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Apoptosis / drug effects
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Apoptosis / physiology*
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Apoptosis / radiation effects
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Cell Cycle / drug effects
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Cell Cycle / physiology
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Cell Cycle / radiation effects
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DNA Damage / drug effects
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DNA Damage / physiology*
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DNA Damage / radiation effects
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DNA Repair / drug effects
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DNA Repair / physiology*
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DNA Repair / radiation effects
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DNA, Mitochondrial / metabolism
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Epigenesis, Genetic / physiology
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Humans
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Mitochondria / drug effects
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Mitochondria / physiology*
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Mitochondria / radiation effects
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Signal Transduction / radiation effects
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Tumor Suppressor Protein p53 / metabolism
Substances
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DNA, Mitochondrial
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Proto-Oncogene Proteins c-bcl-2
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Tumor Suppressor Protein p53