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Background Recent studies have disputed the association between bisphenol A (BPA) and endometriosis. This updated meta-analysis was conducted to investigate the impact of BPA exposure on endometriosis. Methods This study evaluated BPA exposure and endometriosis risk, analyzing studies from Web of Science, PubMed, Embase, Cochrane Library, and Chinese databases (CNKI, CBM, Wanfang, VIP) through August 2025. Methodological quality was assessed via the Newcastle-Ottawa Scale (NOS) and the Agency for Healthcare Research and Quality Tool (AHRQ). Heterogeneity was quantified using I 2 statistics. Pooled odds ratios (ORs) and 95% CIs were calculated using fixed- or random-effects models according to heterogeneity. Subgroup analysis, sensitivity analysis, and publication bias assessment were supplemented to validate the overall finding. Results Seven studies comprising 2,488 participants were included in quantitative synthesis. The meta-analyses demonstrated that BPA exposure was associated with a statistically significant increase in endometriosis risk (OR = 1.36, 95% CI = 1.13–1.63, p = 0.008). Additionally, subgroup analysis indicated that BPA exposure may further elevate endometriosis risk in cases with different regions, populations, and measurement methods. Sensitivity analysis confirmed that the results of these meta-analyses were relatively robust. No publication bias was detected. Systematic review registration https://www.crd.york.ac.uk/PROSPERO/view/CRD420251019552 , identifier PROSPERO (CRD420251019552).

Patients with cholangiocarcinoma have poor clinical outcomes due to late diagnoses, poor prognoses, and limited treatment strategies. To identify drug combinations for this disease, we have conducted a genome-wide CRISPR screen anchored on the bromodomain and extraterminal domain (BET) PROTAC degrader ARV825, from which we identified anticancer synergy when combined with genetic ablation of members of the mTOR pathway. This combination effect was validated using multiple pharmacological BET and mTOR inhibitors, accompanied by increased levels of apoptosis and cell cycle arrest. In a xenograft model, combined BET degradation and mTOR inhibition induced tumor regression. Mechanistically, the 2 inhibitor classes converged on H3K27ac-marked epigenetic suppression of the serine glycine one carbon (SGOC) metabolism pathway, including the key enzymes PHGDH and PSAT1. Knockdown of PSAT1 was sufficient to replicate synergy with single-agent inhibition of either BET or mTOR. Our results tie together epigenetic regulation, metabolism, and apoptosis induction as key therapeutic targets for further exploration in this underserved disease.