ArticleTranslational oncology2026
Multi-scale evidence chain: Linking environmental BPA exposure to ovarian cancer through integrated omics and experimental models.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Bisphenol A and ovarian cancer: emerging evidence and potential biological mechanisms.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
backgroundOvarian cancer (OC) is a leading cause of female cancer mortality. Beyond genetic and reproductive risk factors, emerging evidence suggests bisphenol A (BPA), a widespread endocrine-disrupting chemical, may contribute to ovarian carcinogenesis, though underlying mechanisms remain unclear.
methodsWe employed a multi-dimensional approach combining: (1) cross-sectional NHANES analysis (66 OC cases, 291 matched controls), (2) two-sample Mendelian randomization using GWAS data, (3) integrative bioinformatics (target prediction, nine GEO datasets, WGCNA, machine learning), (4) molecular docking/dynamics simulations, and (5) functional assays in SKOV3 cells.
resultsUrinary BPA levels were significantly elevated in OC patients (p < 0.05).Mendelian randomization suggested a positive association consistent with a potential causal effect (OR=1.25, p = 0.029). Five hub genes (LCN2, LIPA, NR3C1, NR3C2, PGR) were identified across algorithms, showing stable BPA binding in simulations. Single-cell analysis revealed enriched signatures in malignant epithelial cells (p = 0.009). Functional assays confirmed BPA promoted OC proliferation, migration, and invasion (p < 0.05).
conclusionThis integrated analysis provides multi-omic evidence supporting an association between BPA exposure and OC pathogenesis, with MR findings suggesting a potential causal relationship that requires independent replication, identifying five hub genes as potential biomarkers and therapeutic targets.
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