What does this research mean for the field?

CD36+ circulating tumor cells (CTCs) drive immune evasion and metastasis in PD-1-resistant non-small cell lung cancer (NSCLC) through fatty acid oxidation-dependent metabolic reprogramming. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To explore the role of CD36-mediated fatty acid oxidation in immune evasion and metastasis in NSCLC.

February 19, 2026

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CD36-Mediated Fatty Acid Oxidation in CTCs Drives Immune Evasion and Metastasis in NSCLC

HZHuizhen ZhuZhejiang Chinese Medical University SDShuiyan DaiQuzhou City People's Hospital FWFengping WangWenzhou Medical University

Key Points

To explore the role of CD36-mediated fatty acid oxidation in immune evasion and metastasis in NSCLC.
Analyzed CD36 expression in circulating tumor cells (CTCs)
Assessed metabolic reprogramming linked to fatty acid oxidation
Examined immune response in PD-1-resistant NSCLC
Identified CD36+ CTCs as a driver of immune evasion
Demonstrated fatty acid oxidation as a key metabolic pathway
Suggested that targeting this pathway may improve immunotherapy outcomes

Abstract

CD36+ CTCs drive immune evasion and metastasis in PD-1-resistant NSCLC through FAO-dependent metabolic reprogramming. Targeting this metabolic vulnerability may enhance the efficacy of immunotherapy.

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CD36-Mediated Fatty Acid Oxidation in CTCs Drives Immune Evasion and Metastasis in NSCLC

Key Points

Abstract

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