ArticleFrontiers in oncology2026
Single-cell transcriptomics reveals cellular heterogeneity and neoadjuvant chemotherapy response signatures in triple-negative breast cancer.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Triple-negative breast cancer (TNBC) shows marked intratumoral heterogeneity and variable responses to neoadjuvant chemotherapy (NAC), but the cellular determinants of treatment response remain incompletely defined. Methods: We analyzed the scRNA-seq dataset GSE161529 to characterize TNBC cellular states and used bulk cohorts, including GSE25066 and GSE58812, for NAC response-related signature evaluation and clinical validation. Cell types and subtypes were identified by t-SNE clustering. A permutation-based NACR score estimated chemotherapy-response potential. Differentiation hierarchies were reconstructed using CytoTRACE 2 and Monocle 2, and cell-cell communication was inferred with CellChat. Prognostic value was evaluated by Kaplan-Meier analysis, drug sensitivity was predicted using pRRophetic/GDSC, and Results: Nine major cell populations were identified, with cancer cells (49.3%) showing the highest NACR scores. Four cancer cell subtypes were delineated: C2 was enriched in predicted NACR-high groups, whereas C3/C4 correlated with low predicted response. Three tumor-associated macrophage (TAM) subtypes were identified, with TAMs + SLPI associated with high predicted NACR and TAMs + CXCL9 with low predicted NACR. Pseudotime analysis revealed increasing NACR scores along the cancer cell trajectory (C4 to C2) and decreasing scores along the TAM trajectory. Predicted NACR-high tumors showed dominant CAF-cancer cell interactions, whereas predicted NACR-low tumors showed endothelial cell-CAF/TAM communication via PDGFB-PDGFRB and ICAM2-ITGAM/ITGB2. The NACR signature was associated with overall survival (log-rank p = 0.034). Conclusions: This integrative analysis identifies response-associated cancer cell and TAM states and nominates PDGFB-PDGFRB signaling as a candidate resistance-associated pathway, providing potential biomarkers and therapeutic targets for precision TNBC therapy.
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