Mechanism for Synthetic Lethality in BRCA-Deficient Cancers: No Longer Lagging Behind

Mol Cell. 2018 Sep 20;71(6):877-878. doi: 10.1016/j.molcel.2018.08.045.

Abstract

Two recent studies implicate PARP as sensors of incompletely processed Okazaki fragments, changing our view about how single-strand breaks arise in unperturbed cells. Unligated Okazaki fragments may trigger homologous recombination-mediated repair and underpin genome instability in BRCA1/BRCA2-deficient cancers.

Publication types

  • Comment

MeSH terms

  • BRCA1 Protein / genetics
  • BRCA2 Protein / genetics
  • Breast Neoplasms*
  • DNA
  • DNA Repair
  • DNA Replication
  • Humans
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Poly(ADP-ribose) Polymerases*
  • Synthetic Lethal Mutations

Substances

  • BRCA1 Protein
  • BRCA2 Protein
  • Okazaki fragments
  • Poly(ADP-ribose) Polymerase Inhibitors
  • DNA
  • Poly(ADP-ribose) Polymerases