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The leaked plasma components themselves act as potent inflammatory stimuli, recruiting neutrophils and monocytes from the peripheral circulation to infiltrate the brain parenchyma through the compromised BBB (168)
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Concretely, APOC2-K70la stabilizes APOC2 and promotes extracellular lipolysis in NSCLC cell lines, thus leading to free fatty acid release, regulatory T-cell accumulation, immunotherapy resistance, and metastasis in NSCLC
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