The publication titled “Genetic separation of Brca1 functions reveal mutation-dependent Pol Theta vulnerabilities” explores the relationship between Brca1 and Polymerase Theta. We use transgenic mouse models to uncover how specific Brca1 activities in homologous recombination repair impact the dependence on Pol Theta mediated end joining repair, potentially providing new insights into which patients may best respond in the ongoing Pol Theta inhibitor clinical trials.
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