Abstract
Emerging data suggests that synthetic lethal interactions between mutated oncogenes/tumor suppressor genes and molecules involved in DNA damage signaling and repair can be therapeutically exploited to preferentially kill tumor cells. In this review, we discuss the concept of synthetic lethality, and describe several recent examples in which this concept was successfully implemented to target tumor cells in culture, in mouse models, and in human cancer patients.
Publication types
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Research Support, N.I.H., Extramural
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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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Ataxia Telangiectasia Mutated Proteins
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BRCA1 Protein / metabolism
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BRCA2 Protein / metabolism
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Cell Cycle Proteins / metabolism
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DNA Damage
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DNA Repair
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DNA-Binding Proteins / metabolism
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Humans
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Mice
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Neoplasms / genetics
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Neoplasms / therapy*
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Oncogenes / genetics*
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Poly(ADP-ribose) Polymerases / metabolism
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Protein Serine-Threonine Kinases / metabolism
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Tumor Suppressor Protein p53 / genetics*
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Tumor Suppressor Protein p53 / metabolism
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Tumor Suppressor Proteins / metabolism
Substances
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BRCA1 Protein
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BRCA2 Protein
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Cell Cycle Proteins
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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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Poly(ADP-ribose) Polymerases
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ATM protein, human
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Ataxia Telangiectasia Mutated Proteins
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Atm protein, mouse
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Protein Serine-Threonine Kinases