Overcoming immunotherapy resistance in triple-negative breast cancer: a critical review of mast cell plasticity, metabolic reprogramming, and organoid models - Summary - MDSpire
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Overcoming immunotherapy resistance in triple-negative breast cancer: a critical review of mast cell plasticity, metabolic reprogramming, and organoid models
To evaluate current evidence on how mast cell plasticity and metabolic reprogramming contribute to immunotherapy resistance in TNBC.
Key Findings:
Mast cells exhibit high phenotypic diversity, with apMCs capable of priming anti-tumor T cell responses.
Metabolic dysregulation in TNBC skews mast cells towards immunosuppressive phenotypes.
A vicious cycle exists where metabolic reprogramming drives immunosuppression, reinforcing metabolic dysfunction.
Patient-derived organoid models allow for real-time investigation of metabolism-immune interactions.
Interpretation:
The interplay between mast cell plasticity and metabolic changes is crucial for understanding immunotherapy resistance in TNBC.
Limitations:
Current models may not fully replicate the complexity of the human tumor immune microenvironment.
Further research is needed to translate findings from organoid systems into clinical practice.
Conclusion:
Integrating insights from immuno-oncology, cancer metabolism, and bioengineering may lead to actionable strategies to overcome immunotherapy resistance in TNBC.
