ArticleGenes2025
Multi-Modal Profiling Reveals SERPINB3-Driven Immune Evasion and Stromal Immune Mimicry in Triple-Negative Breast Cancer.
Article in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Tumor-Intrinsic DNA Damage Signaling Is Associated with MHC-I Expression and CD8 Cytotoxic T-Cell Engagement in Triple-Negative Breast Cancer.Current issues in molecular biology · 2026Article
- Integrative Single-Cell and Bulk Transcriptomic Analyses with Spatial Validation Identify a Residual Fatty Acid-EMT Subset Driving Chemotherapy Resistance in Triple-Negative Breast Cancer via MIF- and MK-Mediated Ligand-Receptor Signaling.International journal of molecular sciences · 2026Article
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesTriple-negative breast cancer (TNBC) exhibits high immune infiltration yet remains clinically aggressive. Although immune checkpoint blockade benefits a subset of patients, the molecular programs enabling concurrent immune activation and immune evasion in TNBC are not fully defined. This study aimed to identify TNBC-specific tumor-intrinsic and tumor-extrinsic molecular features that may explain this paradox.
methodsPublicly available single-cell RNA-sequencing data from primary breast tumors were analyzed to characterize subtype-specific transcriptional programs across epithelial and stromal compartments. Tumor-intrinsic findings were independently validated using bulk transcriptomic and clinical data from the METABRIC cohort. Tumor microenvironment remodeling was evaluated using multiplexed tissue imaging of TNBC tumors. Functional analyses were done included Gene Ontology enrichment, Hallmark gene set enrichment analysis, and SERPINB3-centered protein-protein interaction network analysis using STRING.
resultsSingle-cell analysis identified
conclusionsTogether, these data indicate that TNBC exhibits co-existing immune activation and immune-suppressive features. The identified epithelial and stromal signatures represent candidate biomarkers that may inform future studies of immune regulation and therapeutic stratification in TNBC.
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