Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Arachidonic Acid Metabolism in PMN-MDSCs Suppresses Antitumor Capacity of T Cells in KRAS-Mutant Cholangiocarcinoma.

Cancer discovery - 1 Sept 2026

Lin Jian, Sang Chen, Xiang Bin, Shen Xia, Zhao Junmei, Xu Shengshi, Pan Jiaomeng, Lin Youpei, Dong Liangqing, Chu Qianqian, Shi Guoming, Zhou Jian, Fan Jia, Zhang Mao, Gao Qiang

Abstract excerpt

Metabolic reprogramming within the tumor microenvironment (TME) impairs antitumor immunity and compromises the efficacy of immunotherapy. Through multiomics-based metabolic subtyping in intrahepatic cholangiocarcinoma, we identified a subgroup with the worst prognosis that demonstrates significant enrichment in both cyclooxygenase/arachidonic acid (COX/AA) metabolism and KRAS mutations. Mechanistically, KRAS...

Read the complete abstract on PubMed

Topics

Humans
Cholangiocarcinoma
Animals
Mice
Myeloid-Derived Suppressor Cells
Proto-Oncogene Proteins p21(ras)

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Arachidonic Acid

Mutation

Tumor Microenvironment

Dinoprostone

Bile Duct Neoplasms

Source

Identifiers

PMID: 41949259
DOI: 10.1158/2159-8290.CD-25-1844

Genes

KRAS
CXCL5
CXCR2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 23 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Arachidonic Acid Metabolism in PMN-MDSCs Suppresses Antitumor Capacity of T Cells in KRAS-Mutant Cholangiocarcinoma.PMID 41949259Read ↗

Demystifying metabolic‒immune crosstalk: how amino acid metabolic reprogramming shapes the malignant phenotype and macrophage polarization of biliary and pancreatic tumors.Semantic proximity Read ↗

Pan-cancer analysis of cholesterol metabolism reveals the uptake as a modulator of tumor immune features and of the KRAS pathway.Semantic proximity Read ↗

New molecular mechanisms in cholangiocarcinoma: signals triggering interleukin-6 production in tumor cells and KRAS co-opted epigenetic mediators driving metabolic reprogrammingSemantic proximity Read ↗

Tumor-associated macrophages in cholangiocarcinoma: complex interplay and potential therapeutic targetSemantic proximity Read ↗

Fatty acids in the tumor microenvironment reprogram neutrophils to induce immunosuppression via adenosineSemantic proximity Read ↗

Multiomics analysis reveals metabolic subtypes and identifies diacylglycerol kinase α (DGKA) as a potential therapeutic target for intrahepatic cholangiocarcinomaSemantic proximity Read ↗

Selective Targeting uPAR-driven Neutrophil Extracellular Traps Functional Clusters to Attenuate Tumor Progression and Enhance the Response to Immunotherapy in Intrahepatic CholangiocarcinomaSemantic proximity Read ↗

Multi-omic Characterization of Pancreatic Cancer-Associated Macrophage Polarization Reveals Deregulated Metabolic Programs Driven by the GMCSF-PI3K PathwaySemantic proximity Read ↗

Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic programs driven by the GM-CSF–PI3K pathwaySemantic proximity Read ↗

Integrative multiomics enhancer activity profiling identifies therapeutic vulnerabilities in cholangiocarcinoma of different etiologiesSemantic proximity Read ↗

Early Infiltration of Innate Immune Cells to the Liver Depletes HNF4α and Promotes Extrahepatic CarcinogenesisSemantic proximity Read ↗

Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor MicroenvironmentSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.