ArticleProceedings of the National Academy of Sciences of the United States of America2011
Rapid growth of a hepatocellular carcinoma and the driving mutations revealed by cell-population genetic analysis of whole-genome data.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 127 citations in OpenAlex.
- Decoding Genomic Diversity to Guide Tumor Lesion-Specific Treatment of Multifocal Hepatocellular Carcinoma.Cancer medicine · 2025Article
- Transcriptome analysis creates a new era of precision medicine for managing recurrent hepatocellular carcinoma.World journal of gastroenterology · 2023Review
- Population genetics of clonally transmissible cancers.Nature ecology & evolution · 2022Review
- Molecular pathogenesis and systemic therapies for hepatocellular carcinoma.Nature cancer · 2022Review
- Review
- Ras Mitogen-activated Protein Kinase Signaling and Kinase Suppressor of Ras as Therapeutic Targets for Hepatocellular Carcinoma.Journal of liver cancer · 2021Review
- The Mutational and Transcriptional Landscapes of Hepatocarcinogenesis in a Rat Model.iScience · 2020Article
- Evolving insights: how DNA repair pathways impact cancer evolution.Cancer biology & medicine · 2020Review
- Implications of driver genes associated with a high tumor mutation burden identified using next-generation sequencing on immunotherapy in hepatocellular carcinoma.Oncology letters · 2020Article
- Circ-TCF4.85 silencing inhibits cancer progression through microRNA-486-5p-targeted inhibition of ABCF2 in hepatocellular carcinoma.Molecular oncology · 2020Article
- Efficient Tumor Clearance and Diversified Immunity through Neoepitope Vaccines and Combinatorial Immunotherapy.Cancer immunology research · 2019Article
- Tumorigenesis as the Paradigm of Quasi-neutral Molecular Evolution.Molecular biology and evolution · 2019Article
- Identifying Clonal Origin of Multifocal Hepatocellular Carcinoma and Its Clinical Implications.Clinical and translational gastroenterology · 2019Review
- DSMNC: a database of somatic mutations in normal cells.Nucleic acids research · 2019Article
- Long Non-Coding RNA NEAT1 Promoted Hepatocellular Carcinoma Cell Proliferation and Reduced Apoptosis Through the Regulation of Let-7b-IGF-1R Axis.OncoTargets and therapy · 2019Article
- Diagnostic and therapeutic potential of the gut microbiota in patients with early hepatocellular carcinoma.Therapeutic advances in medical oncology · 2019Review
- Advances in genomic hepatocellular carcinoma research.GigaScience · 2018Review
- Article
- Host and Viral Genetic Variation in HBV-Related Hepatocellular Carcinoma.Frontiers in genetics · 2018Review
- Spatio-Temporal Genomic Heterogeneity, Phylogeny, and Metastatic Evolution in Salivary Adenoid Cystic Carcinoma.Journal of the National Cancer Institute · 2017Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
44 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We present the analysis of the evolution of tumors in a case of hepatocellular carcinoma. This case is particularly informative about cancer growth dynamics and the underlying driving mutations. We sampled nine different sections from three tumors and seven more sections from the adjacent nontumor tissues. Selected sections were subjected to exon as well as whole-genome sequencing. Putative somatic mutations were then individually validated across all 9 tumor and 7 nontumor sections. Among the mutations validated, 24 were amino acid changes; in addition, 22 large indels/copy number variants (>1 Mb) were detected. These somatic mutations define four evolutionary lineages among tumor cells. Separate evolution and expansion of these lineages were recent and rapid, each apparently having only one lineage-specific protein-coding mutation. Hence, by using a cell-population genetic definition, this approach identified three coding changes (CCNG1, P62, and an indel/fusion gene) as tumor driver mutations. These three mutations, affecting cell cycle control and apoptosis, are functionally distinct from mutations that accumulated earlier, many of which are involved in inflammation/immunity or cell anchoring. These distinct functions of mutations at different stages may reflect the genetic interactions underlying tumor growth.
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