ArticleiLIVER2024
Targeting hepatocellular carcinoma growth and metabolism: A synergistic approach with para-toluenesulfonamide and radiofrequency ablation.
Article in iLIVER, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Pralatrexate represses the resistance of HCC cells to molecular targeted agents via the miRNA-34a/Notch pathway.Discover oncology · 2024Article
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and aims: Hepatocellular carcinoma (HCC) is one of the most prevalent and lethal forms of cancer, posing challenges to standard treatment methods. Radiofrequency ablation (RFA) has emerged as a valuable technique for the local control of advanced HCC, especially in cases unsuitable for surgical resection. Para-toluenesulfonamide (PTS) has demonstrated antitumor properties in various cancers, yet its efficacy against HCC remains underexplored. The present study aims to investigate the therapeutic potential of PTS in HCC and examine potential synergistic effects with RFA. Methods: PTS was injected directly into subcutaneous tumor tissues and its effects on cell survival, gene expression, and metabolic activity in HCC cells were evaluated. The effect of PTS and RFA in combination on HCC growth was examined using a nude mouse model of subcutaneous HCC. Data were visualized using heat maps. Results: PTS inhibited the survival of HCC cells in a dose-dependent manner, modulating the expression of key genes related to cell survival, apoptosis, epithelial-mesenchymal transition, and proliferation. The combination of PTS and RFA markedly enhanced the inhibition of HCC tumor growth and induced alterations in cellular metabolism. Conclusion: Combining PTS and RFA may be a promising approach to improve the efficacy of HCC treatment.
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Registered trials
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