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Inherited mutations in  BRCA1 ,  BRCA2 , and  PALB2  cause a high risk of breast cancer. Here, we conducted parallel conditional knockout (CKO) of  Brca1 ,  Palb2 , and  Brca2 , individually and in combination, along with one copy of  Trp53 , in the mammary gland of nulliparous female mice. We observed a functional equivalence of the three genes in their basic tumor-suppressive activity, a linear epistasis of  Palb2  and  Brca2 , but complementary roles of  Brca1  and  Palb2  in mammary tumor suppression, as combined ablation of either  Palb2  or  Brca2  with  Brca1  led to delayed tumor formation. Whole-exome sequencing (WES) revealed both similarities and differences between  Brca1  and  Palb2  or  Brca2  null tumors. Analyses of mouse mammary glands and cultured human cells showed that combined loss of BRCA1 and PALB2 led to high levels of reactive oxygen species (ROS) and increased apoptosis, implicating oxidative stress in the delayed tumor development in  Brca1 ; Palb2  double CKO mice. The functional complementarity between BRCA1 and PALB2/BRCA2 and the role of ROS in tumorigenesis require further investigation.

Genetic interactions among Brca1, Brca2, Palb2, and Trp53 in mammary tumor development