Objective:

To synthesize current evidence on how immune–tumor cell ligand-receptor axes drive metabolic adaptation and therapeutic resistance across cancers, highlighting their significance in improving treatment outcomes.

Approach:

Key Findings:

• Immune–tumor ligand–receptor axes actively drive tumor metabolic reprogramming, influencing therapeutic outcomes.
• Lactate signaling, macrophage-derived inflammatory cues, and checkpoint-associated pathways are key regulators of immune suppression and metabolic adaptation.
• Targeting immune–tumor communication alongside metabolic dependencies may help overcome resistant tumor niches and improve treatment efficacy.

Interpretation:

Therapeutic resistance is influenced by dynamic interactions within the tumor microenvironment, particularly through ligand-receptor signaling.

Limitations:

• The review does not provide specific clinical trial data or outcomes related to the discussed mechanisms; further research is needed to translate these findings into effective therapeutic strategies.

Conclusion:

Understanding immune-tumor communication systems may offer new opportunities to disrupt resistant tumor ecosystems and improve the durability of cancer therapy, potentially transforming clinical practice.

Attribution Notice

This content is an AI-generated, fully rewritten summary based on a published scholarly article. It does not reproduce the original text and is not a substitute for the original publication. Readers are encouraged to consult the source for full context, data, and methodology.