ArticleExperimental dermatology2026
PI3Kγ Deficiency Suppresses Cutaneous Squamous Cell Carcinoma Formation by Modulating the Tumour Microenvironment Rather Than by Directly Regulating Keratinocyte Proliferation.
Article in Experimental dermatology, 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.
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Authors and funding
11 authors.
Funding
Abstract
Phosphatidylinositol-3 kinase (PI3K) is a central regulator of cell proliferation, survival, metabolism, and migration via the downstream AKT/mTOR pathway. Although activating mutations in the catalytic subunit of PI3Kα (p110α) have been documented in various cancers, including cutaneous squamous cell carcinoma (cSCC), the role of PI3Kγ (p110γ), which is predominantly expressed in immune cells, remains poorly defined in cSCC. To elucidate the function of p110γ in cSCC development, we compared tumour formation in wild-type and p110γ-deficient mice using both a chemical carcinogenesis model and a syngeneic cSCC cell implantation model. While genetic deletion or pharmacological inhibition of PI3Kγ did not affect keratinocyte proliferation or migration in vitro, p110γ-deficient mice exhibited significantly delayed tumour onset, reduced tumour burden, and suppressed growth of implanted cSCC tumours in vivo. Immunohistochemical analyses revealed that total CD4
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