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A Mendelian randomization study identifies three specific immune cell traits as causal risk factors for intrahepatic cholangiocarcinoma. The analysis, published by Zhipeng Ye in 2026, suggests N-acetylleucine and fructosyllysine as potential metabolic mediators. Experimental validation in HuCC-T1 and RBE cell lines showed that disrupting the DLAT-leucine metabolic axis impaired tumor cell proliferation and migration.
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