ArticleCellular and molecular gastroenterology and hepatology2026
Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation.
Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Development and Validation of a Crotonylation-Related Prognostic Risk Model for Cholangiocarcinoma Based on Integrative Transcriptome Analysis.Digestive diseases and sciences · 2026Article
- Opening the Flood Gates: Epigenetic Regulators Safeguard Against Rogue Lineage Plasticity in Cholangiocarcinoma.Cellular and molecular gastroenterology and hepatology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsThe SWI/SNF ATP-dependent chromatin remodeling complex regulates transcriptional machinery access and is critical in normal physiology and cancer development. PBRM1, a key subunit of this complex, is frequently mutated in intrahepatic cholangiocarcinoma (iCCA). This study aims to explore the role of PBRM1 in liver physiology and its involvement in iCCA development.
methodsLiver-specific Pbrm1 knockout (Pbrm1 KO) mice were generated to assess the effects of Pbrm1 loss under various conditions. These mice were exposed to a 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet to induce cholestatic injury and were also subjected to a high-fat diet to evaluate susceptibility to liver steatosis. Chromatin accessibility and gene expression under both normal and injury conditions were examined. Additionally, the impact of Pbrm1 loss was analyzed in combination with an activating Kras
resultsPbrm1 KO mice exhibited increased susceptibility to cholestatic injury, with an enhanced ductular reaction. Loss of Pbrm1 reduced chromatin accessibility at hepatocyte-specific and metabolically important genes, although RNA expression remained unaffected during homeostasis. Following cholestatic injury, hepatocyte-specific gene expression was significantly reduced compared with wild-type controls. Pbrm1 KO mice also showed heightened vulnerability to high-fat diet-induced liver steatosis. When combined with Kras
conclusionsPBRM1 maintains chromatin accessibility for hepatocyte differentiation-related genes. Its loss promotes differentiation toward cholangiocytes during injury or tumorigenesis, driving iCCA development.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.