BRCA1, PARP, and 53BP1: Conditional synthetic lethality and synthetic viability

Amal Aly, Shridar Ganesan

Research output: Contribution to journalArticlepeer-review

82 Scopus citations


BRCA1 plays a critical role in the regulation of homologous recombination (HR)-mediated DNA double-strand break repair. BRCA1-deficient cancers have evolved to tolerate loss of BRCA1 function. This renders them vulnerable to agents, such as PARP inhibitors, that are conditionally 'synthetic lethal' with their underlying repair defect. Recent studies demonstrate that BRCA1-deficient cells may acquire resistance to these agents by partially correcting their defect in HR-mediated repair, either through reversion mutations in BRCA1 or through 'synthetic viable' loss of 53BP1. These findings and their clinical implications will be reviewed in this article.

Original languageEnglish (US)
Pages (from-to)66-74
Number of pages9
JournalJournal of molecular cell biology
Issue number1
StatePublished - Feb 1 2011

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Cell Biology


  • 53BP1
  • BRCA1
  • DNA repair
  • PARP


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