ASO Author Reflections: Broaden the Targeted Population of Synthetic Lethality for Taiwanese Breast Cancer.
Where this comes from
- Record sourced from PubMed, PMID 35391610.
- Also identified by DOI 10.1245/s10434-022-11407-5.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Poly(ADP-ribose) polymerase (PARP) inhibitors selectively cause the failure of DNA single-stranded break (SSB) repair but do not affect double-stranded break (DSB) repair. Furthermore, antitumor activities have been reported for breast cancer, with germline BRCA1/2 mutations. The prevalence of germline BRCA1/2 mutations never exceed one-tenth; beyond BRCA1/2, genes recurrently altered (more than 5%) in the homologous repair pathway are ARID1A, PALB2, and PTEN. Altered homologous recombination repair genes can total up to one-quarter based on different definitions, and the potential of PARP inhibitors will be elucidated when further studies unraveling the impact of individual homologous recombination genes are conducted.