Abstract
Background: Loss-of-function (LOF) alterations in Cyclin-Dependent Kinase 12 (CDK12) are found across tumors, including metastatic prostate (∼5%) and serous ovarian (∼3%) cancers. While initial data suggested that CDK12 LOF compromises DNA repair by homologous recombination (HR), there is burgeoning evidence questioning this notion. CDK12-deficient tumors lack genomic features indicative of HR-deficiency (HRD) and instead harbor large tandem duplications thought to originate from DNA replication stress of unknown etiology.
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