ArticlePloS one2022
Triple-negative breast cancer influences a mixed M1/M2 macrophage phenotype associated with tumor aggressiveness.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- From tumor microenvironment orchestrators to actionable targets: a systematic review of TAM-targeted therapies in triple-negative breast cancer.International journal of clinical oncology · 2026Pooled it
- The tumor microenvironment in triple negative breast cancer and a strategy to improve responses to immunotherapy using cryoablation and immunostimulants.Cancer biology & therapy · 2026Review
- Tumor-educated macrophages promote cytokine-driven lung colonization in triple-negative breast cancer.Oncoimmunology · 2026Article
- The M1/M2 Test System for Determining Macrophage Phenotypes.International journal of molecular sciences · 2026Review
- LyP vs advanced-stage CTCLs: single-cell profiling reveals markers of self-limited vs aggressive disease behavior.Blood advances · 2026Article
- Review
- Inhibition of histone demethylase LSD1 suppresses CD47 expression and enhances efficacy of CD47 blockade in breast cancer.Journal for immunotherapy of cancer · 2026Article
- Culture Dimensionality Regulates Protein Expression and Bioactivity in THP-1-Derived Macrophages.Biomedicines · 2026Article
- MLK4 orchestrates macrophage-induced triple-negative breast cancer invasion and ECM remodeling via enhanced paracrine signaling and NF-κB-MMP axis activation.Cell death & disease · 2026Article
- Extracellular vesicles from canine mammary tumor cells promote macrophage M2 polarization and enhance tumor progression.Veterinary research communications · 2026Article
- Interleukin-6 secreted by tumor-associated macrophages promotes proliferation and migration through JAK2/STAT3 signaling pathway in human prostate cancer cells.Prostate international · 2026Article
- Article
- Targeting the JAK/STAT pathway with isoliquiritigenin in ovarian cancer: molecular mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Inflammatory indexes as prognostic biomarkers in advanced triple negative breast cancer patients.Frontiers in oncology · 2026Article
- Decoding the tumor microenvironment of triple-negative breast cancer: from immune evasion to precision immunotherapy.Frontiers in immunology · 2026Review
- Emerging roles of USP7 in tumor immune evasion, metabolic reprogramming, and therapeutic resistance.Frontiers in immunology · 2026Review
- Quantitative Cell Type-Specific Immunopeptidome Analysis of Macrophage and Tumor Coevolution Reveals Therapeutic MHC-I Peptides in Glioblastoma.Cancer research · 2025Article
- Article
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- Race-related host and microbe transcriptomic signatures in triple-negative breast cancer.NPJ breast cancer · 2025Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is characterized by excessive accumulation of tumor-infiltrating immune cells, including tumor-associated macrophages (TAMs). TAMs consist of a heterogeneous population with high plasticity and are associated with tumor aggressiveness and poor prognosis. Moreover, breast cancer cells can secrete factors that influence TAM polarization. Therefore, this study aimed to evaluate the crosstalk between cancer cells and macrophages in the context of TNBC. Cytokine-polarized M2 macrophage were used as control. Distinct from the classical M2 macrophage, TAMs generated from TNBC-conditioned media upregulated both M1- and M2-associated genes, and secreted both the anti-inflammatory cytokine interleukin IL-10 and the proinflammatory cytokine IL-6 and tumor necrosis factor- α. Theses TNBC-induced TAMs exert aggressive behavior of TNBC cells. Consistently, TCGA and MTABRIC analyses of human breast cancer revealed upregulation of M1- associated genes in TNBC comparing with non-TNBC. Among these M1-associated genes, CXCL10 and IL1B were revealed to be independent prognostic factors for disease progression. In conclusion, TNBC cells induce macrophage polarization with a mixture of M1 and M2 phenotypes. These cancer-induced TAMs further enhance tumor cell growth and aggressiveness.
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