ArticleMedComm2025
A Phosphatidylinositol 3-Kinase Gamma Inhibitor Enhances Anti-Programmed Death-1/Programmed Death Ligand-1 Antitumor Effects by Remodeling the Tumor Immune Microenvironment of Ovarian Cancer.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Single-cell RNA sequencing in ovarian cancer: decoding the tumor microenvironment for personalized therapy.Journal of ovarian research · 2026Review
- TAMs in the Gynecological Tumor Microenvironment: Insights from Cross-Cancer Studies for Immunotherapy.Cancers · 2026Review
- Targeting Tumor-Associated Macrophages to Reshape the Immuno-Mechanical Landscape: Molecular Mechanisms and Therapeutic Strategies.International journal of biological sciences · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that the effectiveness of immune checkpoint blockade in the treatment of ovarian cancer (OC) is poor. A promising small molecule inhibitor targeting phosphatidylinositol 3-kinase gamma (PI3Kγ) has recently been applied in combination with other drugs for tumor treatment. This study aimed to determine whether a PI3Kγ inhibitor can enhance the antitumor effects of anti-programmed death-1/programmed death ligand-1 (anti-PD-1/PD-L1) therapies in OC and to explore the underlying immunomolecular mechanism involved. Changes in the expression of PI3Kγ, PD-1, PD-L1, and tumor-associated macrophages (TAMs) during the progression of OC were detected in clinical tissue samples. We also constructed a coculture system of OC cells with lymphocytes for in vitro study, and a subcutaneous and intraperitoneal implantation OC mouse model was constructed for in vivo studies. OC is an immunosuppressed tumor with predominant infiltration of M2 throughout the entire disease course. We also found that a PI3Kγ inhibitor combined with anti-PD-1 therapy can enhance the antitumor effects of anti-PD-1 agents by modulating the PI3Kγ-AKT-NF-κB pathway, reprogramming TAMs, decreasing the number of myeloid-derived suppressor cells, increasing the number of CD8
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Registered trials
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