title: Loss of 53BP1 is a gain for BRCA1 mutant cells.
abstract: Mutations in BRCA1 predispose to tumorigenesis presumably from the inability to accurately repair DNA double-strand breaks by homologous recombination. Two new papers shed light on how loss of the DNA damage response protein 53BP1 reverses phenotypes of BRCA1 mutant cells, with potential clinical implications.
authors.affiliation: Developmental Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Kass
authors.forename: Mary Ellen
authors.initials: ME
authors.lastname: Moynahan
authors.forename: Maria
authors.initials: M
authors.lastname: Jasin