Abstract
Over the past 20 years, there has been considerable progress in our understanding of the biological functions of the BRCA1 and BRCA2 cancer susceptibility genes. This has led to the development of new therapeutic approaches that target tumours with loss-of-function mutations in either BRCA1 or BRCA2. Tumours that share molecular features of BRCA-mutant tumours - that is, those with 'BRCAness' - may also respond to similar therapeutic approaches. Several paradigm shifts require a reassessment of the concept of BRCAness, how this property is assayed and its relevance to our understanding of tumour biology and the treatment of cancer.
MeSH terms
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Antineoplastic Agents / pharmacology
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BRCA1 Protein / genetics*
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BRCA1 Protein / metabolism
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BRCA2 Protein / genetics*
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BRCA2 Protein / metabolism
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Biomarkers, Tumor / analysis
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Biomarkers, Tumor / genetics
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Drug Resistance, Neoplasm / drug effects
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Drug Resistance, Neoplasm / genetics
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Female
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Genetic Predisposition to Disease
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Germ-Line Mutation
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Humans
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Mutation
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Neoplasms / drug therapy*
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Neoplasms / genetics*
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Phthalazines / pharmacology
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Piperazines / pharmacology
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Poly(ADP-ribose) Polymerase Inhibitors / pharmacology
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Rad51 Recombinase / genetics
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Rad51 Recombinase / metabolism
Substances
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Antineoplastic Agents
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BRCA1 Protein
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BRCA1 protein, human
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BRCA2 Protein
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BRCA2 protein, human
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Biomarkers, Tumor
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Phthalazines
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Piperazines
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Poly(ADP-ribose) Polymerase Inhibitors
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RAD51 protein, human
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Rad51 Recombinase
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olaparib