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We integrated massively parallel reporter assays (MPRA), chromatin profiling, and network analysis to identify estrogen-responsive breast cancer variants. Screening 1,604 GWAS-identified breast cancer variants identified 73 estrogen-modulated SNVs (emSNVs). Chromatin accessibility modeling validated allele-specific effects, identifying variants that disrupt pioneer factor binding to chromatin and others that modulate transcription factor (TF) recruitment to pre-accessible enhancers. emSNV targets converged on pathways including mitochondrial metabolism, NF-\u03baB signaling, and chromatin regulation. Aggregating emSNVs into a polygenic risk score (PRS\n                  <jats:sub>E2<\/jats:sub>\n                  ) revealed interactions with reproductive risk factors in 13,026 post-menopausal BRCA cases and 108,265 controls, including age at first birth (p=0.0052); a control PRS lacking estrogen-responsive variants showed no interactions. This framework bridges molecular and epidemiological GxE studies to uncover variants whose disease associations depend on environmental context, with implications for understanding polygenic disease risk.\n                <\/jats:p>","DOI":"10.64898\/2026.09.09.26362309","type":"posted-content","created":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T04:20:24Z","timestamp":1789186824000},"source":"Crossref","is-referenced-by-count":0,"title":["Estrogen interactions with breast cancer risk variants in regulatory DNA"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9951-9974","authenticated-orcid":false,"given":"Ibtihal","family":"Elfaki","sequence":"first","affiliation":[{"name":"Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305 USA"},{"name":"Program in Epithelial Biology, Stanford University, Stanford, CA, 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