ArticleiScience2026
HERV2365 upregulates FGF1 expression by sponging miR-326 to promote the progression of intrahepatic cholangiocarcinoma.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Early Postoperative Outcomes in Patients with Peripheral Artery Disease Residing in Uranium Legacy-Affected Areas: A Comparative Study.Journal of clinical medicine · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrahepatic cholangiocarcinoma (ICC) is an aggressive primary liver cancer with a dismal prognosis, underscoring the need to identify previously unrecognized molecular regulators involved in ICC progression. Although human endogenous retroviruses (HERVs) are aberrantly activated in multiple malignancies, their role in ICC remains poorly defined. Here, through integrative profiling of bulk and single-cell transcriptomes, we identified HERV2365 as a key upregulated oncogenic factor, which was enriched in ICC malignant cells and associated with poor prognosis. Functional assays demonstrated that HERV2365 enhanced ICC proliferation and tumorigenesis both
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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.