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One of the mysteries of ovarian cancer is why is it that chromosomes with a mutation causing defective DNA repair, such as found with BRCA mutations promote cancer cell growth? Usually defective cells are removed as part of the normal stasis or equilibrium of tissue renewal.
With the ready availability of whole genome sequencing it has become clear that homologous recombination deficiency (HRD) of BRCA is complex with multiple other sites of structural change with replication and adhesion or annealing of the DNA strands. The effect of these other abnormalities is to compensate for the defective DNA repair with other pathways to correct the faulty DNA thereby enabling survival of cancer cells that would normally be destroyed.
Discovery of these multiple compensatory mutations may lead to better targeted therapy and possibly the correction of the basic defective mechanism with prevention of subsequent cancer.
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