Comprehensive genomic analyses of patient samples revealed
virtually unstudied cyclin-dependent kinase 12 (Cdk12) as a novel
candidate in ovarian tumorigenesis. Our recent study determined that Cdk12
maintains genome stability via regulation of transcription of key
DNA-damage response genes including BRCA1, ATR and FANCI; pointing this
kinase to be a novel tumor suppressor and a potential drug target.
However, precise molecular mechanisms leading to the Cdk12-dependent
ovarian tumorigenesis are unknown. The goal of this project is to achieve
an initial molecular understanding of these deregulations; this could
eventually lead to development of novel therapeutic approaches for ovarian
cancer.