ReviewActa pharmaceutica Sinica. B2026
Targeting cytokine/chemokine signaling to convert immunologically cold tumors into hot: Emerging strategies in cancer immunotherapy.
Review in Acta pharmaceutica Sinica. B, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
5 authors.
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Abstract
The field of cancer immunotherapy has undergone significant advancements in recent years, leading to a paradigm shift in treatment methodologies. However, "cold" tumors, characterized by low immune cell infiltration and an immunosuppressive tumor microenvironment (TME), present considerable therapeutic challenges. In contrast to "hot" tumors, which exhibit vigorous immune activity and responsiveness to immune checkpoint inhibitors, "cold" tumors evade immune surveillance through mechanisms such as impaired antigen expression and restricted T-lymphocyte infiltration. This immune evasion is closely linked to the dysregulation of cytokines and chemokines, which shape the TME and orchestrate immune responses. This review delineates the immune escape mechanisms of cold tumors, with particular emphasis on the role of cytokines/chemokines in modulating the TME. Here we will explore advanced therapeutic strategies that employ engineered chemokines/cytokines (
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