An in vitro model of CDH1 mutated ER-positive breast cancer demonstrates that NF1 knockdown confers a growth advantage in the presence of 4-hydroxy tamoxifen.
In AA women, significant ARTP gene-level associations included CDH1 with LN+ (p<sub>ARTP</sub> = 0.10; multi-allelic OR = 1.13, 95%CI 1.07-1.19, p<sub>FDR</sub> = 0.0003) and SIPA1 with ER- breast cancer (p<sub>ARTP</sub> = 0.10; multi-allelic OR = 1.16, 95%CI 1.02-1.31, p<sub>FDR</sub> = 0.03).
Gene-based analyses revealed that CDH1 was responsible for the pathway association (P < 0.01), with rs4783673 in CDH1 statistically significant after gene-level adjustment for multiple comparisons (P = 9.2×10(-5), corrected P = 0.02). rs142697907 in PTPN14 was associated with ER-positive breast cancer and rs2456773 in CDK1 with ER-negativity in case-only analysis after gene-level correction for multiple comparisons (corrected P < 0.05).