ArticleBreast cancer research : BCR2025
Obesity is a major modifiable factor associated with ER-negative breast cancer: epidemiological and mechanistic evidence from a high-risk cohort.
Article in Breast cancer research : BCR, 2025. 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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1 citing paper in PubMed.
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5 authors.
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Abstract
backgroundThe biological mechanisms linking modifiable risk factors to aggressive breast cancer subtypes remain poorly defined, particularly in underrepresented populations which experience a disproportionate burden. Regions with high obesity prevalence and early-onset disease provide a unique setting to investigate these drivers.
methodsIn a case–control study of 567 premenopausal breast cancer cases and 906 controls from a high-risk population, tumors were classified into molecular subtypes. Logistic regression estimated subtype-specific risks, and population-attributable fractions (PAF) were calculated. To provide mechanistic validation, we examined paracrine effects of fibroblasts from obese versus lean women on ER-α expression in breast epithelial cells using co-culture and qRT-PCR analysis.
resultsObesity was the strongest modifiable factor, with adjusted ORs ranging from 2.29 (luminal B) to 4.32 (TNBC), corresponding to a population-attributable fraction of approximately 43% for TNBC—an effect size exceeding most previous reports. Family history was independently associated with TNBC. Mechanistically, primary mammary fibroblasts from obese donors downregulated ER-α and HER2 in human mammary epithelial cells, providing a plausible explanation for obesity-driven ER/HER2-negative tumorigenesis.
conclusionsObesity is a major, modifiable factor strongly associated with TNBC, with its effect magnified in high-risk populations. The mechanistic link to ER and HER2 suppression suggests a plausible biological pathway, highlighting metabolic health as a critical target for prevention strategies worldwide.
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