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In the last few years, the resurrection of platinum drugs in breast cancer has been due to a belief that certain subsets of the disease are particularly sensitive to these agents as a result of having impaired capacity to repair DNA damage. Specifically, homologous repair (HR) is a mechanism whereby cells are able to repair double strand breaks that can be caused by environmental insults or inherent errors. Intact BRCA1 and BRCA2 genes play a role in HR, but in patients with BRCA-mutated breast tumors, HR can be impaired, making these cells particularly sensitive to platinum chemotherapy agents and PARP inhibitors.
To determine whether specific genomic or mutational signatures can predict which patients are most likely to respond to platinum…