ArticleNature communications2023
Organoid models of fibrolamellar carcinoma mutations reveal hepatocyte transdifferentiation through cooperative BAP1 and PRKAR2A loss.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Liver Organoids: From Disease Modelling to Regenerative Medicine.Cell proliferation · 2026Review
- Review
- Targeting the LINC01272-FUS signal axis inhibits the migration and invasion of testicular germ cell tumors.Cancer cell international · 2025Article
- Article
- Mouse radial spoke 3 is a metabolic and regulatory hub in cilia.Nature structural & molecular biology · 2025Article
- Expression of DNAJB1-PRKACA oncogene suppresses the differentiation potential of liver progenitor organoids towards a hepatocyte lineage.Scientific reports · 2025Article
- Emerging biotechnologies for engineering liver organoids.Bioactive materials · 2025Review
- Morphomolecular Pathology and Genomic Insights into the Cells of Origin of Cholangiocarcinoma and Combined Hepatocellular-Cholangiocarcinoma.The American journal of pathology · 2025Review
- DNAJB1-PRKACA Fusion Drives Fibrolamellar Liver Cancer through Impaired SIK Signaling and CRTC2/p300-Mediated Transcriptional Reprogramming.Cancer discovery · 2025Article
- Clinical applications of human organoids.Nature medicine · 2025Review
- Tumor organoids for primary liver cancers: A systematic review of current applications in diagnostics, disease modeling, and drug screening.JHEP reports : innovation in hepatology · 2024Article
- Expanded detection and impact ofNAR cancer · 2024Article
- Article
- Organoid as a promising tool for primary liver cancer research: a comprehensive review.Cell & bioscience · 2024Review
- Mapping of mitogen and metabolic sensitivity in organoids defines requirements for human hepatocyte growth.Nature communications · 2024Article
- Recruitment of BAG2 to DNAJ-PKAc scaffolds promotes cell survival and resistance to drug-induced apoptosis in fibrolamellar carcinoma.Cell reports · 2024Article
- cAMP-PKA/EPAC signaling and cancer: the interplay in tumor microenvironment.Journal of hematology & oncology · 2024Review
- Models of fibrolamellar carcinomas, tools for evaluation of a new era of treatments.Frontiers in immunology · 2024Review
- Human organoids-on-chips for biomedical research and applications.Theranostics · 2024Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrolamellar carcinoma (FLC) is a lethal primary liver cancer, affecting young patients in absence of chronic liver disease. Molecular understanding of FLC tumorigenesis is limited, partly due to the scarcity of experimental models. Here, we CRISPR-engineer human hepatocyte organoids to recreate different FLC backgrounds, including the predominant genetic alteration, the DNAJB1-PRKACA fusion, as well as a recently reported background of FLC-like tumors, encompassing inactivating mutations of BAP1 and PRKAR2A. Phenotypic characterizations and comparisons with primary FLC tumor samples revealed mutant organoid-tumor similarities. All FLC mutations caused hepatocyte dedifferentiation, yet only combined loss of BAP1 and PRKAR2A resulted in hepatocyte transdifferentiation into liver ductal/progenitor-like cells that could exclusively grow in a ductal cell environment. BAP1-mutant hepatocytes represent primed cells attempting to proliferate in this cAMP-stimulating environment, but require concomitant PRKAR2A loss to overcome cell cycle arrest. In all analyses, DNAJB1-PRKACA
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