ArticleClinical and translational medicine2026
Multi-omics analysis identifies PUS7 as an immune modulator driving NETs-mediated macrophage polarization in pancreatic cancer.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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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Who cites it
3 citing papers in PubMed.
- Pseudouridine synthase 7 as a context-specific therapeutic target in cancer.The Journal of pharmacology and experimental therapeutics · 2026Review
- Multi-omics analysis identifies PUS7 as an immune modulator driving NETs-mediated macrophage polarization in pancreatic cancer.Clinical and translational medicine · 2026Article
- Caught in the NET: A Review on the Emerging Role of Neutrophil Extracellular Traps in PDAC Development.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Pseudouridine synthases (PUS) have been implicated in various cancers, yet their roles in pancreatic cancer immunity remain unclear. Through integrative multi-omics analyses combining genomics, transcriptomics, and clinical datasets, we evaluated associations between PUS family genes and oncogenic features, including tumour microenvironment scores, immune infiltration, cancer stemness, and prognosis. Among them, PUS7 and PUS3 showed the strongest correlations with tumour-promoting phenotypes, with high PUS7 expression in PDAC predicting poor overall survival. Functional assays revealed that PUS7 overexpression markedly enhanced PDAC cell proliferation, migration, and invasion. Transcriptomic profiling demonstrated that PUS7 promotes neutrophil extracellular traps formation, identifying it as a key regulator of NET-mediated immune modulation. Single-cell RNA sequencing of orthotopic mouse models showed PUS7 overexpression reduced macrophage infiltration and skewed macrophage polarization towards the M2 phenotype while suppressing M1 polarization. We found that PUS7 reshapes the PDAC immune landscape primarily by inducing NETs, which drive macrophage polarization from M1 to M2, fostering immune suppression and tumour progression. The PUS7-NET-M2/M1 axis thus represents a novel mechanism of PDAC pathogenesis and a potential therapeutic target in this lethal malignancy. HIGHLIGHTS: PUS7 enhances pancreatic ductal adenocarcinoma progression by modulating the tumour immune microenvironment. PUS7 induces neutrophil extracellular trap formation within pancreatic tumours. NETs reprogram tumour-associated macrophages from an M1 to an M2 phenotype, promoting immune suppression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.