ArticleAdvanced healthcare materials2026
Injectable Thermosensitive Hydrogel Targeting STAT3 Reprograms Neutrophils to Amplify Anti-Tumor Immunity Post-Radiofrequency Ablation in HCC.
Article in Advanced healthcare materials, 2026. 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.
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Who cites it
1 citing paper in PubMed.
- Targeting the CRYAB/β-Catenin Axis with an MMP-9-Responsive Hydrogel Disrupts CTC Clusters to Suppress Progression of Hepatocellular Carcinoma after Radiofrequency Ablation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Radiofrequency ablation (RFA) for hepatocellular carcinoma (HCC) carries a high risk of recurrence due to residual tumors and the immunosuppressive tumor microenvironment. This study identifies that incomplete RFA activates the JAK2/STAT3 pathway in tumor-associated neutrophils (TANs), polarizing them toward immunosuppressive phenotypes. In vitro, icaritin (ICT) inhibits TAN survival and migration, and reverses the immunosuppressive phenotype by suppressing STAT3 phosphorylation. To enable localized delivery, we developed an injectable hydrogel (HP@ICT) by leveraging the interfacial complexation of hydroxypropyl-β-cyclodextrin and the thermosensitive gelation of poloxamer 407. It is injected via the ablation needle into the residual cavity and undergoes in situ gelation, overcoming post-ablation drug delivery barriers to enable sustained release of ICT. In vivo, HP@ICT effectively suppresses immunosuppressive TANs, reduces the proportion of PMN-MDSCs, and promotes the infiltration and activation of CD8
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