A transposon mutagenesis screen indicates that loss of 53BP1 expression rescues the clonal growth defect of BRCA1 null cells. 53BP1 deficiency is shown to abrogate the cell cycle arrest triggered in the absence of BRCA1 and to partially restore homologous recombination. The potential clinical implications of these findings are supported by the reduction of 53BP1 expression in sporadic triple-negative and BRCA-associated breast cancers.
- Peter Bouwman
- Amal Aly
- Jos Jonkers