ArticleCommunications biology2024
Characterization of tumor evolution by functional clonality and phylogenetics in hepatocellular carcinoma.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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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.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Enteroviral epitope mimicry enables NK cell-mediated targeting of ASPH in hepatocellular carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Evaluation of tumor clonality with chemical carcinogenesis in a mouse model of visualized X chromosome inactivation.Journal of toxicologic pathology · 2026Article
- A Medical Anthropology Assessment of Community Liver Cancer Risks: Qualitative Comparisons of Communities with Different Risk Profiles in Thailand.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Developments and Applications of Liver-on-a-Chip Technology-Current Status and Future Prospects.Biomedicines · 2025Review
- Cancer immune evasion, immunoediting and intratumour heterogeneity.Nature reviews. Immunology · 2025Review
- Exploring Aerobic Energy Metabolism in Breast Cancer: A Mutational Profile of Glycolysis and Oxidative Phosphorylation.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
21 authors at 9 institutions in 2 countries.
Funding
Abstract
Hepatocellular carcinoma (HCC) is a molecularly heterogeneous solid malignancy, and its fitness may be shaped by how its tumor cells evolve. However, ability to monitor tumor cell evolution is hampered by the presence of numerous passenger mutations that do not provide any biological consequences. Here we develop a strategy to determine the tumor clonality of three independent HCC cohorts of 524 patients with diverse etiologies and race/ethnicity by utilizing somatic mutations in cancer driver genes. We identify two main types of tumor evolution, i.e., linear, and non-linear models where non-linear type could be further divided into classes, which we call shallow branching and deep branching. We find that linear evolving HCC is less aggressive than other types. GTF2IRD2B mutations are enriched in HCC with linear evolution, while TP53 mutations are the most frequent genetic alterations in HCC with non-linear models. Furthermore, we observe significant B cell enrichment in linear trees compared to non-linear trees suggesting the need for further research to uncover potential variations in immune cell types within genomically determined phylogeny types. These results hint at the possibility that tumor cells and their microenvironment may collectively influence the tumor evolution process.
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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.