ArticleHepatobiliary surgery and nutrition2026
EREG-secreting THBS1
Article in Hepatobiliary surgery and nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- CD177Gut · 2026Article
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) is an important surgical treatment for unresectable liver tumors, while with its mechanism remaining unclear. We aim to comprehensively examine the key immune cells that induce the rapid liver regeneration during the ALPPS procedure and unearth the relevant mechanism(s) in patients with hepatocellular carcinoma (HCC). Methods: Matched ALPPS stage I and II liver tissues were collected from five HCC patients and subjected to cytometry by time-of-flight (CyTOF) and single-cell RNA sequencing (scRNA-seq) analysis. Peripheral blood samples were collected during subsequent routine clinical examinations to explore the dynamic changes in circulating immune cells and cytokines. The changes in the transcription profiles of liver tissues between ALPPS stage I and II were explored by bulk RNA-seq analysis. Tissue microarrays containing paired tissues from another 22 HCC patients who underwent ALPPS were constructed for validation. Results: The CyTOF data revealed an increase in tissue monocytes during the ALPPS-induced liver regeneration (from 13.36% to 29.78%, P=0.04). There was also a shift from a macrophage-enriched to monocyte-enriched local immune environment in the remnant liver tissues induced by ALPPS. The scRNA-seq analysis identified that a cluster of THBS1 Conclusions: The ALPPS procedure induced activation of the complement system in hepatocytes, specifically increasing the expression of C5a, which led to the recruitment of THBS1
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