Targeting TRIM37-driven centrosome dysfunction in 17q23-amplified breast cancer.

ABSTRACT: Genomic instability is a hallmark of cancer, and has a central role in the initiation and development of breast cancer^1,2. The success of poly-ADP ribose polymerase inhibitors in the treatment of breast cancers that are deficient in homologous recombination exemplifies the utility of synthetically lethal genetic interactions in the treatment of breast cancers that are driven by genomic instability³. Given that defects in homologous recombination are present in only a subset of breast cancers, there is a need to identify additional driver mechanisms for genomic instability and targeted strategies to exploit these defects in the treatment of cancer. Here we show that centrosome depletion induces synthetic lethality in cancer cells that contain the 17q23 amplicon, a recu

SUBMITTER: Yeow ZY 

PROVIDER: S-EPMC7597367 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature