ReviewFrontiers in oncology2025
Immunotherapy resistance in triple-negative breast cancer: Molecular mechanisms, tumor microenvironment, and therapeutic implications.
Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed.
- Estrogen Receptors and Enzymes Involved in Estrogen Synthesis as Breast Cancer Treatment Targets.International journal of molecular sciences · 2026Review
- Breast Cancer: Epidemiology, Molecular Classification, Diagnostics and Evolving Treatment Paradigms.Molecules (Basel, Switzerland) · 2026Review
- Review
- Review
- Overcoming Resistance in Triple-Negative Breast Cancer: A Translational Perspective on Next-Generation DNA Damage Response Inhibitors and Synthetic Lethality.Molecules (Basel, Switzerland) · 2026Review
- Single-cell RNA sequencing reveals immune microenvironment heterogeneity in BRCA1-mutated and sporadic triple-negative breast cancer.Translational oncology · 2026Article
- Anthraquinone-Loaded Liposomes for TAM Reprogramming in Triple-Negative Breast Cancer: Mechanistic Rationale, Delivery Logic, and Translational Challenges.Pharmaceutics · 2026Review
- Therapeutic targeting of RAGE/STAT3 signaling abrogates S100A7-driven breast tumorigenicity and immune suppression.Breast cancer research : BCR · 2026Article
- Targeting Autophagy to Overcome Chemoresistance and Immune Resistance in Triple-Negative Breast Cancer.Cancers · 2026Review
- Integrative immunogenomic and experimental characterization reveals CXCL9, CXCL13, CCL5 and CD74 as key oncogenic drivers in breast cancer.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Review
- DUSP1: Triple-Negative Breast Cancer and Therapeutic Potential.Current oncology (Toronto, Ont.) · 2026Review
- Advances and challenges in biomarker guided management of triple-negative breast cancer in the era of neoadjuvant chemo-immunotherapy.Frontiers in oncology · 2026Review
- Triple-negative breast cancer: current understanding and future perspectives.Exploration of targeted anti-tumor therapy · 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
- Reprogramming the immunosuppressive breast cancer microenvironment: integrating cellular, metabolic, and stromal targets for rational immunotherapy.Frontiers in immunology · 2026Review
- Assessing the prognostic role of androgen receptor expression in non-metastatic triple-negative breast cancer.Frontiers in oncology · 2026Article
- Graph neural networks for multi-scale gene-drug interaction modeling in cancer: applications, challenges, and therapeutic opportunities for breast cancer drug resistance.Frontiers in oncology · 2026Review
- Metastatic Triple Negative Breast Cancer: Navigating a Rapidly Evolving Therapeutic Landscape.Oncology research · 2026Review
- PD-L1 targeting in triple negative breast cancer: in silico and in vitro validation of wasp venom peptide MP-1.Medical oncology (Northwood, London, England) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is a unique subtype of breast cancer characterized by high invasiveness, high metastasis rates, and poor prognosis, making it an important focus within global malignancies. Due to the absence of estrogen receptor, progesterone receptor, and HER2 expression, TNBC presents significant challenges in treatment. Metastatic progression markedly increases treatment complexity, drastically reducing patient survival rates. The metastatic and drug resistance processes of TNBC involve complex, multi-step biological mechanisms regulated through various molecular mechanisms and signaling pathways within and outside tumor cells. In recent years, immunotherapy has brought new hope for TNBC. Compared to other breast cancer subtypes, TNBC demonstrates higher immunogenicity, often accumulating a higher mutational burden that generates more neoantigens, thus typically resulting in a tumor microenvironment (TME) enriched with tumor-infiltrating lymphocytes (TILs). Additionally, PD-L1 expression is significantly higher in TNBC compared to other subtypes, closely correlating with TIL abundance. These characteristics position TNBC as a strong candidate for immune checkpoint inhibitor (ICI) therapy. Clinical trials have demonstrated promising efficacy of ICIs in TNBC, overturning previous beliefs that breast cancer is generally insensitive to immunotherapy. This review summarizes recent advances regarding resistance types, molecular mechanisms, associated genes and pathways, the role of the tumor microenvironment, and clinical strategies related to immunotherapy resistance in the neoadjuvant setting of TNBC, aiming to provide insights and guidance for future research exploration and clinical practice.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.