ArticleNature biotechnology2009
A conditional transposon-based insertional mutagenesis screen for genes associated with mouse hepatocellular carcinoma.
Article in Nature biotechnology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
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Who cites it
133 citing papers in PubMed, 200 citations in OpenAlex.
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- Mfap4: a promising target for enhanced liver regeneration and chronic liver disease treatment.NPJ Regenerative medicine · 2023Article
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- Non-viral chimeric antigen receptor (CAR) T cells going viral.Immuno-oncology technology · 2023Review
- DNA Deamination Is Required for Human APOBEC3A-Driven Hepatocellular Carcinoma In Vivo.International journal of molecular sciences · 2023Article
- Ring Finger Protein 125 Is an Anti-Proliferative Tumor Suppressor in Hepatocellular Carcinoma.Cancers · 2022Article
- Genetic and Cellular Contributions to Liver Regeneration.Cold Spring Harbor perspectives in biology · 2021Article
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- Exploring liver cancer biology through functional genetic screens.Nature reviews. Gastroenterology & hepatology · 2021Review
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- Identification of cancer driver genes using Sleeping Beauty transposon mutagenesis.Cancer science · 2021Review
73 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 10 institutions in 3 countries.
Funding
Abstract
We describe a system that permits conditional mobilization of a Sleeping Beauty (SB) transposase allele by Cre recombinase to induce cancer specifically in a tissue of interest. To demonstrate its potential for developing tissue-specific models of cancer in mice, we limit SB transposition to the liver by placing Cre expression under the control of an albumin enhancer/promoter sequence and screen for hepatocellular carcinoma (HCC)-associated genes. From 8,060 nonredundant insertions cloned from 68 tumor nodules and comparative analysis with data from human HCC samples, we identify 19 loci strongly implicated in causing HCC. These encode genes, such as EGFR and MET, previously associated with HCC and others, such as UBE2H, that are potential new targets for treating this neoplasm. Our system, which could be modified to drive transposon-based insertional mutagenesis wherever tissue-specific Cre expression is possible, promises to enhance understanding of cancer genomes and identify new targets for therapeutic development.
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Registered trials
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