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Sequencing nearly 500 high-grade serous ovarian cancers showed that almost all carry TP53 mutations and about half have defects in homologous recombination DNA repair, the biology that PARP inhibitors exploit.
Integrated genomic analysis by The Cancer Genome Atlas of 489 high-grade serous ovarian adenocarcinomas, finding TP53 mutations in 96 percent, germline or somatic BRCA1/2 mutations in about 20 percent, homologous recombination defects in about half, widespread copy-number changes, and four transcriptional subtypes.
The homologous recombination deficiency concept, and the case for testing all high-grade serous cancers for BRCA and related defects, come from this dataset.