ArticleBiology2025
Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast Cancer.
Article in Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
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Who cites it
2 citing papers in PubMed.
- Integrative bioinformatics identifies NSCLC biomarkers associated with LPS metabolism and circadian disruption.Translational oncology · 2026Article
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5 authors.
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Abstract
The urgent need for novel therapeutic strategies in triple-negative breast cancer (TNBC)-characterized by absent ER, PR, and HER2 expression-stems from its association with a paucity of effective treatments and an adverse prognosis. This study identifies TNFRSF12A as a key gene specifically overexpressed in TNBC versus other subtypes. Validation with clinical specimens confirmed its exclusive upregulation in TNBC tissues, correlating significantly with worse patient outcomes. Functional enrichment analysis (STRING/DAVID) indicated TNFRSF12A's primary involvement in pathways positively regulating cell migration, angiogenesis, and hypoxia response. Immune infiltration profiling (TIMER/TISCH2) revealed selective enrichment of TNFRSF12A in cancer-associated fibroblasts (CAFs). Its expression showed a significant positive correlation with the CAF marker FAP (ρ = 0.304) and CAF infiltration levels, but inverse correlations with CD8
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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 Socratic graph.