ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Replacing BPA: Structural Substitutes BPAF Binding to the Progesterone Receptor Elevates Breast Cancer Risk.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Replacing BPA: Structural Substitutes BPAF Binding to the Progesterone Receptor Elevates Breast Cancer Risk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
As the global production of bisphenol analogs (BPs) surges to replace regulated bisphenol A (BPA), their pervasive environmental presence and uncharacterized breast cancer risk raise critical public health concerns. Herein, the environmental risks of BPs are deciphered by linking their structural affinity for the progesterone receptor (PR), a master regulator of breast cancer, to oncogenic outcomes across experimental tiers. Molecular simulations reveal that environmental BPAF and BPB exhibited stronger binding to the PR-ligand binding domain (LBD) than BPA. Chemical assays confirm persistent PR-LBD structural changes after BPs exposure, mimicking endocrine disruption patterns. The cellular thermal shift assay also confirms the interaction between the PR and BPs. In vitro, BPAF and BPF boost PR expression at human-relevant concentrations. In addition, BPAF elevates PR expression, and the enhanced migratory and invasive capacities are effectively suppressed by the PR inhibitor. Toxicological Prioritization Index-based risk stratification, weighted by the binding affinity of BPs to the PR and cellular toxicity, ranks BPAF as the highest-risk analog. Alarmingly, low-dose BPAF exposure (30 µg kg
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.