ArticleDiscover oncology2025
Genetic evidence for causal effects of inflammatory protein factors on breast cancer.
Article in Discover oncology, 2025. 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
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Immune system, inflammatory response, and regulated cell death in breast cancer research (Review).Oncology reports · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundBreast cancer (BC) represents a significant public health challenge characterized by complex pathogenic mechanisms. While inflammatory proteins are known to play crucial roles in cancer development, their causal relationships with breast cancer risk remain inadequately understood. This study employed Mendelian randomization (MR) analysis to investigate potential causal associations between inflammatory proteins and breast cancer susceptibility.
methodsWe utilized genome-wide association study (GWAS) data for inflammatory protein levels from 14,824 European individuals as exposure data. The primary outcome data were obtained from BC GWAS summary statistics, with an additional independent BC cohort serving as validation(FinnGen_R12). The primary analysis was conducted using inverse-variance weighted (IVW) method, supplemented by MR-Egger and weighted median approaches. Comprehensive sensitivity analyses included Cochran's Q test, MR-Egger intercept test, MR-PRESSO, and leave-one-out analysis. The causal direction was verified through Steiger test and reverse MR. We further performed multivariable MR (MVMR), linkage disequilibrium score regression (LDSC), and colocalization analysis to strengthen our findings.
resultsAfter Bonferroni correction, we identified a significant inverse genetic association between Leukemia inhibitory factor receptor (LIFR) levels and BC risk. While C-X-C motif chemokine 5 (CXCL5) did not survive Bonferroni correction, it showed significant negative association with BC in MVMR analysis. Reverse MR analyses found no evidence of causal effects of BC on these inflammatory proteins, supporting the direction of our primary findings. Colocalization analysis revealed strong evidence of shared genetic variants between LIFR and BC, suggesting common genetic determinants underlying their relationship.
conclusionThis study provides genetic evidence for causal relationships between inflammatory proteins and BC risk, particularly highlighting the protective role of LIFR. These findings enhance our understanding of BC pathogenesis and may inform future therapeutic strategies.
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Registered trials
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