When we began our studies, it was expected that BRG1 was a weak tumor suppressor in mammary gland because about 10% of Brg1+/− mice eventually developed mammary tumors (61, 62) and because there were functional interactions between BRG1 and cell cycle regulatory proteins, including RB and p53 (30, 42, 81). This tentative identification of BRG1 as a mammary tumor suppressor was challenged by our work (59) and by others (55). The conditional knockout of Brg1 in the mouse mammary gland did not cause mammary tumors (63). We observed that fewer than 2% of BRG1 sequences in the TCGA database contained mutations. Breast cancer is not alone in this requirement for BRG1. BRG1 is also required for the proliferation of HeLa cells and mouse fibroblasts (82, 83).
