ArticleProceedings of the National Academy of Sciences of the United States of America2007
Distinct pathways of genomic progression to benign and malignant tumors of the liver.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 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
136 citing papers in PubMed, 216 citations in OpenAlex.
- Met Receptor Tyrosine Kinase and Chemoprevention of Oral Cancer.Journal of the National Cancer Institute · 2018Trial
- Adaptive oncogenesis of β-catenin emerges from declining liver tissue integrity.Nature communications · 2026Article
- Histone deacetylase enzyme activity is not the universal anticancer target of HDAC inhibitors.Signal transduction and targeted therapy · 2026Article
- Chronic stress disrupts hepatic homeostasis and accelerates liver cancer progression through ADRB2 signaling.Science advances · 2026Article
- Bmi1 represses HLF to drive the formation and development of intrahepatic cholangiocarcinoma.British journal of cancer · 2026Article
- Development of a cyst-targeted therapy for polycystic kidney disease using an antagonistic dimeric IgA monoclonal antibody against cMET.Cell reports. Medicine · 2025Article
- Transcriptomics assisted by metabolomics analysis provides insights into regulation mechanisms during carcinogenic process in a hydrodynamically transfected liver cancer model.Cancer cell international · 2025Article
- Chemoprevention of hepatocellular carcinoma using N-acetylgalactosamine-conjugated siRNAs.Disease models & mechanisms · 2025Article
- RBM39 promotes hepatocarcinogenesis by regulating RFX1's alternative splicing and subsequent activation of integrin signaling pathway.Oncogene · 2025Article
- Suppression of Hepatocellular Carcinoma by Deletion of SIRT2 in Hepatocytes via Elevated C/EBPβ/GADD45γ.Cellular and molecular gastroenterology and hepatology · 2025Article
- Oncogenic plasmid DNA and liver injury agent dictates liver cancer development in a mouse model.Clinical science (London, England : 1979) · 2024Article
- Preclinical Models of Hepatocellular Carcinoma: Current Utility, Limitations, and Challenges.Biomedicines · 2024Review
- Synthesis of (2The Journal of organic chemistry · 2024Article
- TRIM45 facilitates NASH-progressed HCC by promoting fatty acid synthesis via catalyzing FABP5 ubiquitylation.Oncogene · 2024Article
- Hydrodynamic Transfection of Hepatocytes for the Study of Hepatocellular Carcinogenesis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Dynamic regulation of EXO1 promotes the progression from liver fibrosis to HCC through TGF-β1/Smad signaling feedback loop.Hepatology communications · 2024Article
- Increased hsa-miR-100-5p Expression Improves Hepatocellular Carcinoma Prognosis in the Asian Population withCancers · 2023Article
- New and Old Key Players in Liver Cancer.International journal of molecular sciences · 2023Review
- Article
- An overview of mouse models of hepatocellular carcinoma.Infectious agents and cancer · 2023Review
76 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
We used several of the genetic lesions commonly associated with human liver tumors to reconstruct genetic progression to hepatocellular carcinoma and adenoma in mouse models. We initiated tumorigenesis with a transgene of the protooncogene MET or by hydrodynamic transfection of MET in combination with other genes into the livers of adult animals. Hepatocellular carcinoma in both instances arose from cooperation between MET and constitutively active versions of beta-catenin. In contrast, adenomas were produced by cooperation between MET and defective signaling through the transcription factor HNF1alpha. Prompted by these findings, we uncovered a coincidence between activation of the protein-tyrosine kinase encoded by MET and activating mutations of beta-catenin in a subset of human hepatocellular carcinomas. Inactivation of MET transgenes led to regression of hepatocellular carcinomas despite the persistence of activated beta-catenin. The tumors eventually recurred in the absence of MET expression, however, presumably after the occurrence of one or more events that cooperated with activated beta-catenin in lieu of MET. These results offer insight into hepatic tumorigenesis, provide mouse models that should be useful in the further study of hepatic tumorigenesis and for preclinical testing, and identify a subset of human hepatocellular carcinomas that may be susceptible to combination therapy directed against Met and the Wnt signaling pathway.
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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 OpenQuestion graph.