ArticleScience advances2021
PD-1 independent of PD-L1 ligation promotes glioblastoma growth through the NFκB pathway.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 35 citations in OpenAlex.
- Spatial single-cell profiling identifies protein kinase Cδ-expressing microglia with anti-tumor function in glioblastoma.iScience · 2026Article
- Meningeal immunity and "Interstitial" therapy: a new paradigm for immunotherapy in glioblastoma.Frontiers in immunology · 2026Review
- Pembrolizumab promotes degradation of cyclin dependent kinase 6 and suppresses ovarian cancer progression in vitro.Scientific reports · 2025Article
- Negative Immune Checkpoint Inhibitors.Pharmaceutics · 2025Review
- TIM-3 teams up with PD-1 in cancer immunotherapy: mechanisms and perspectives.Molecular biomedicine · 2025Review
- Programmed cell death protein 1 in cancer cells.Cell communication and signaling : CCS · 2025Review
- Unlocking the mystery of the PD-1/PD-L1 axis: beyond the checkpoint hype.Frontiers in immunology · 2025Review
- PD-1 interactome in osteosarcoma: identification of a novel PD-1/AXL interaction conserved between humans and dogs.Cell communication and signaling : CCS · 2024Article
- Immune Characteristics and Immunotherapy of HIV-Associated Lymphoma.Current issues in molecular biology · 2024Review
- Type I interferon signaling induces melanoma cell-intrinsic PD-1 and its inhibition antagonizes immune checkpoint blockade.Nature communications · 2024Article
- Tumor cell-intrinsic PD-1 promotes Merkel cell carcinoma growth by activating downstream mTOR-mitochondrial ROS signaling.Science advances · 2024Article
- Cancer Stem Cells in Tumours of the Central Nervous System in Children: A Comprehensive Review.Cancers · 2023Review
- Detecting monocyte trafficking in an animal model of glioblastoma using RCancer immunology, immunotherapy : CII · 2023Article
- Targeting Lin28 axis enhances glypican-3-CAR T cell efficacy against hepatic tumor initiating cell population.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Traditional Chinese medicine inhibits PD-1/PD-L1 axis to sensitize cancer immunotherapy: a literature review.Frontiers in oncology · 2023Review
- Effects of postoperative radiotherapy and docetaxel and PD-1 inhibitors on the survival and safety of glioblastoma patients: a systematic review and meta-analysis.Annals of translational medicine · 2022Article
- Distinct antibody clones detect PD-1 checkpoint expression and block PD-L1 interactions on live murine melanoma cells.Scientific reports · 2022Article
- The immune landscape of high-grade brain tumor after treatment with immune checkpoint blockade.Frontiers in immunology · 2022Article
- Perspectives of metal-organic framework nanosystem to overcome tumor drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain tumor–initiating cells (BTICs) drive glioblastoma growth through not fully understood mechanisms. Here, we found that about 8% of cells within the human glioblastoma microenvironment coexpress programmed cell death 1 (PD-1) and BTIC marker. Gain- or loss-of-function studies revealed that tumor-intrinsic PD-1 promoted proliferation and self-renewal of BTICs. Phosphorylation of tyrosines within the cytoplasmic tail of PD-1 recruited Src homology 2–containing phosphatase 2 and activated the nuclear factor kB in BTICs. Notably, the tumor-intrinsic promoting effects of PD-1 did not require programmed cell death ligand 1(PD-L1) ligation; thus, the therapeutic antibodies inhibiting PD-1/PD-L1 interaction could not overcome the growth advantage of PD-1 in BTICs. Last, BTIC-intrinsic PD-1 accelerated intracranial tumor growth, and this occurred in mice lacking T and B cells. These findings point to a critical role for PD-1 in BTICs and uncover a nonimmune resistance mechanism of patients with glioblastoma to PD-1– or PD-L1–blocking therapies.
Identifiers
What OpenQuestion holds
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.