S. Cigall Kadoch

Nov 11, 2024 | nature.com | Carman Man-Chung Li |Francesca Silvestri |Nomeda Girnius |Aviv Regev |Alyssa Cordes |S. Cigall Kadoch

AbstractGermline BRCA1 mutation carriers face a high breast cancer risk; however, the underlying mechanisms for this risk are not completely understood. Using a new genetically engineered mouse model of germline Brca1 heterozygosity, we demonstrate that early tumor onset in a Brca1 heterozygous background cannot be fully explained by the conventional ‘two-hit’ hypothesis, suggesting the existence of inherent tumor-promoting alterations in the Brca1 heterozygous state.