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Article

KRAS mutation-driven O-GlcNAcylation of CLDN18.2 enhances the progression of pancreatic cancer and reduces the efficacy of CLDN18.2-targeted therapy.

Gut - 12 May 2026

Liu Jing, Hou Xupeng, Li Lin, Bai Weiwei, Zhou Tianxing, Chen Moran, Yu Hu, Sun Hongxia, Xu Tingting, Wang Yifei, Chang Antao, Feng Yukuan, Yu Jun, Huang Chongbiao, Xie Yongjie, Hao Jihui

Abstract excerpt

BACKGROUND: CLDN18.2 has emerged as a promising therapeutic target in gastric and gastro-oesophageal junction cancers. However, its clinical efficacy in pancreatic ductal adenocarcinoma (PDAC) has been modest, suggesting the presence of regulatory mechanisms impairing its efficacy. OBJECTIVE: We aim to investigate how O-linked N-acetylglucosaminylation (O-GlcNAcylation) affects CLDN18.2 subcellular localisation,...

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Identifiers

PMID: 41513443
DOI: 10.1136/gutjnl-2025-336277

Genes

CLDN18
KRAS

Variants

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

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