ArticlePloS one2025
Molecular determinants of neoadjuvant chemotherapy resistance in breast cancer: An analysis of gene expression and tumor microenvironment.
Article in PloS one, 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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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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Who cites it
2 citing papers in PubMed.
- Pathological Complete Response After Neoadjuvant Chemotherapy in Breast Cancer: A Literature Overview.Cancers · 2026Review
- Overcoming immunotherapy resistance in triple-negative breast cancer: a critical review of mast cell plasticity, metabolic reprogramming, and organoid models.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Neoadjuvant chemotherapy (NAC) is a critical component of breast cancer treatment, but the molecular mechanisms underlying resistance remain poorly understood. This study aimed to identify transcriptomic changes associated with NAC resistance across four breast cancer subtypes: Luminal A, Luminal B/HER2-positive, Luminal B/HER2-negative, and Triple-Negative Breast Cancer (TNBC). RNA-seq analysis was performed on paired pre- and post-NAC breast cancer samples from 32 non-responders. Differentially expressed genes (DEGs) were identified, and functional enrichment analyses were conducted. Protein-protein interaction (PPI) networks were constructed to identify hub genes. Tumor microenvironment (TME) infiltration was estimated using deconvolution algorithms. The results revealed distinct gene expression profiles between pre- and post-NAC samples, with FOS and NR4A1 being common DEGs across all subtypes. Enriched pathways varied among subtypes, including signal transduction, estrogen biosynthesis, extracellular matrix organization, dendritic cell activation, and B cell activation. TME analysis showed increased infiltration of specific immune cell populations after NAC, including CD4 memory T cells, regulatory T cells, neutrophils, macrophages, and mast cells, varying by subtype. These findings suggest that NAC modulates gene expression, cellular activity, and TME interactions, potentially contributing to treatment resistance. Understanding the molecular determinants of NAC resistance is crucial for developing targeted therapeutic strategies and improving outcomes for breast cancer patients.
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