Targeting tumor-associated macrophages in non-small cell lung cancer: mechanisms, prognosis, and therapeutic opportunities
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View abstract on PubMed
Summary
This summary is machine-generated.Tumor-associated macrophages (TAMs) drive non-small cell lung cancer (NSCLC) growth and resistance. Targeting these M2-like macrophages offers a promising therapeutic strategy for NSCLC precision oncology.
Area Of Science
- Oncology
- Immunology
- Cancer Biology
Background
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer death globally.
- Tumor-associated macrophages (TAMs), especially M2-like phenotypes, are critical regulators of NSCLC progression, metastasis, and treatment resistance.
- TAMs influence tumor growth, angiogenesis, immune evasion, and chemoresistance through various signaling pathways.
Purpose Of The Study
- To comprehensively review the biological functions and mechanistic roles of TAMs in NSCLC.
- To highlight the clinical implications of TAMs as prognostic indicators and therapeutic targets.
- To discuss emerging strategies for targeting TAMs in NSCLC treatment.
Main Methods
- Literature review of studies on TAMs in NSCLC.
- Analysis of TAM functions including immunosuppression, angiogenesis, and epithelial-mesenchymal transition.
- Examination of TAM-mediated immune evasion and chemoresistance mechanisms.
- Review of therapeutic strategies targeting TAMs and associated challenges.
Main Results
- M2-like TAMs promote NSCLC growth, metastasis, and resistance via immunosuppression and other mechanisms.
- TAMs contribute to immune evasion through PD-L1, IL-10, and TGF-β signaling.
- Specific pathways like IL-6/STAT3 and P2X7/STAT6 are implicated in TAM-driven chemoresistance.
- High M2-TAM infiltration correlates with poor prognosis but can paradoxically predict response to PD-1/PD-L1 blockade.
Conclusions
- TAMs play multifaceted roles in NSCLC, impacting tumor progression and treatment response.
- Targeting TAMs presents a promising avenue for NSCLC therapy.
- Challenges including macrophage plasticity and biomarker development need to be addressed for effective TAM-targeted therapies.
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