SynthesisInternational journal of molecular sciences2021
What Do We Have to Know about PD-L1 Expression in Prostate Cancer? A Systematic Literature Review. Part 3: PD-L1, Intracellular Signaling Pathways and Tumor Microenvironment.
Synthesis in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 4 of them syntheses that pooled it.
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Who cites it
28 citing papers in PubMed, 4 syntheses or guidelines pooled it, 38 citations in OpenAlex.
- What Do We Have to Know about PD-L1 Expression in Prostate Cancer? A Systematic Literature Review. Part 5: Epigenetic Regulation of PD-L1.International journal of molecular sciences · 2021Pooled it
- Pooled it
- Pooled it
- What Do We Have to Know about PD-L1 Expression in Prostate Cancer? A Systematic Literature Review. Part 4: Experimental Treatments in Pre-Clinical Studies (Cell Lines and Mouse Models).International journal of molecular sciences · 2021Pooled it
- Tumor‑immune spatiotemporal co‑evolution: A new paradigm for understanding and overcoming therapy resistance in metastatic castration‑resistant prostate cancer (Review).International journal of molecular medicine · 2026Review
- Novel approaches to modulate CAR-T cell function by targeting the tumor microenvironment in ovarian cancer.Journal of ovarian research · 2026Review
- Beta-glucans in oncology: revolutionizing treatment with immune power & tumor targeting.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Exploration of prognosis and immune infiltration characteristics in glioblastoma multiforme based on lipid metabolism related genes.Discover oncology · 2025Article
- Novel hormone therapies for advanced prostate cancer: Understanding and countering drug resistance.Journal of pharmaceutical analysis · 2025Review
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- Bridging Cancer and COVID-19: The Complex Interplay of ACE2 and TMPRSS2.Cancer medicine · 2025Review
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- Machine learning analysis identified NNMT as a potential therapeutic target for hepatocellular carcinoma based on PCD-related genes.Scientific reports · 2025Article
- Post-transarterial chemoembolization hypoxia-induced HIF-1α/WNT/β-catenin signaling promotes hepatocellular carcinoma progression via programed death ligand 1 upregulation.Clinical and experimental immunology · 2025Article
- The role of immunotherapy in targeting tumor microenvironment in genitourinary cancers.Frontiers in immunology · 2025Review
- MDA-MB-231 breast cancer cells adapted to anchorage-independent growth reveal senescent-like phenotype and persistent downregulation of PD-L1 expression.Frontiers in oncology · 2025Article
- Programmed Death Ligand 1 (PD-L1) Expression in Lymphomas: State of the Art.International journal of molecular sciences · 2024Review
- Prostate cancer therapy using immune checkpoint molecules to target recombinant dendritic cells.Investigative and clinical urology · 2024Article
- Androgen Insensitivity Syndrome with Bilateral Gonadal Sertoli Cell Lesions, Sertoli-Leydig Cell Tumor, and Paratesticular Leiomyoma: A Case Report and First Systematic Literature Review.Journal of clinical medicine · 2024Article
- Prognostic value of RNA methylation-related genes in gastric adenocarcinoma based on bioinformatics.PeerJ · 2024Article
Corrections and comments
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Authors and funding
27 authors at 10 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment (TME) includes immune (T, B, NK, dendritic), stromal, mesenchymal, endothelial, adipocytic cells, extracellular matrix, and cytokines/chemokines/soluble factors regulating various intracellular signaling pathways (ISP) in tumor cells. TME influences the survival/progression of prostate cancer (PC), enabling tumor cell immune-evasion also through the activation of the PD-1/PD-L1 axis. We have performed a systematic literature review according to the PRISMA guidelines, to investigate how the PD-1/PD-L1 pathway is influenced by TME and ISPs. Tumor immune-escape mechanisms include suppression/exhaustion of tumor infiltrating cytotoxic T lymphocytes, inhibition of tumor suppressive NK cells, increase in immune-suppressive immune cells (regulatory T, M2 macrophagic, myeloid-derived suppressor, dendritic, stromal, and adipocytic cells). IFN-γ (the most investigated factor), TGF-β, TNF-α, IL-6, IL-17, IL-15, IL-27, complement factor C5a, and other soluble molecules secreted by TME components (and sometimes increased in patients' serum), as well as and hypoxia, influenced the regulation of PD-L1. Experimental studies using human and mouse PC cell lines (derived from either androgen-sensitive or androgen-resistant tumors) revealed that the intracellular ERK/MEK, Akt-mTOR, NF-kB, WNT and JAK/STAT pathways were involved in PD-L1 upregulation in PC. Blocking the PD-1/PD-L1 signaling by using immunotherapy drugs can prevent tumor immune-escape, increasing the anti-tumor activity of immune cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.