ArticleJournal of translational internal medicine2026
Focal adhesion kinase inhibition enhances response to checkpoint immunotherapy in hepatocellular carcinoma.
Article in Journal of translational internal medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Review
- RPRD1A drives lenvatinib resistance in hepatocellular carcinoma via the ITGA5-FAK signaling axis.Molecular biomedicine · 2026Article
- MTHFD1L in muscle invasive bladder cancer: a multi-cohort study on prognosis and therapeutic response.World journal of surgical oncology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and objectives: Despite the remarkable efficacy of immune checkpoint inhibitors (ICIs) in cancer therapy, their clinical benefit in hepatocellular carcinoma (HCC) remains limited. Focal adhesion kinase (FAK) plays a pivotal oncogenic role in various tumors by promoting angiogenesis, tumor proliferation, and immunosuppression. Therefore, targeting FAK represents a promising strategy to enhance immunotherapy outcomes in HCC. Methods: We analyzed RNA-sequencing data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) to compare Results: FAK was highly expressed and frequently amplified in HCC tumors, which predicted worse pathological features of patients. A notable feature of FAK-positive HCC tumors was an adverse immune microenvironment marked by a depletion of CD8 Conclusions: FAK inhibitors can enhance the sensitivity of HCC to anti-PD-1 therapy by inhibiting angiogenesis and fibrosis and promoting CD8
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