ReviewFrontiers in immunology2026
Lipid metabolism and the immune microenvironment in gastric cancer.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
The treatment of gastric cancer (GC) has entered an era of precision medicine combining molecular subtyping, immune checkpoint inhibitors (ICIs), anti-human epidermal growth factor receptor 2 (HER2), anti-claudin 18.2 (CLDN18.2), anti-angiogenic therapy, and chemotherapy. However, efficacy remains limited by tumor microenvironment (TME) heterogeneity, immune exclusion, myeloid suppression, nutrient competition, and metabolic adaptation. Lipid metabolic reprogramming represents a class of mechanisms with high translational value among metabolic immune checkpoints in GC: it supports tumor-cell membrane synthesis, redox homeostasis, peritoneal/omental metastasis, and adaptation to therapeutic stress, while also affecting regulatory T cells (Tregs), tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), dendritic cells, and CD8+ T cells. This review focuses on cluster of differentiation 36 (CD36)-mediated fatty acid uptake; carnitine palmitoyltransferase 1A (CPT1A)-dependent fatty acid oxidation (FAO); fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), sterol regulatory element-binding protein 1 (SREBP-1), and stearoyl-CoA desaturase 1 (SCD1)-mediated
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