ArticleCancer communications (London, England)2023
High baseline tumor burden-associated macrophages promote an immunosuppressive microenvironment and reduce the efficacy of immune checkpoint inhibitors through the IGFBP2-STAT3-PD-L1 pathway.
Article in Cancer communications (London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 43 citations in OpenAlex.
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- Cancer-Associated Fibroblast-Derived FGF7 Promotes Immune Escape in Oral Squamous Cell Carcinoma via JAK/STAT3-Mediated PD-L1 Expression.Molecular carcinogenesis · 2026Article
- Rewiring the tumor microenvironment: IGFBP2 at the Nexus of remodeling and therapy resistance?Biochimica et biophysica acta. Reviews on cancer · 2026Review
- CXCL3 Antagonism Reverses Systemic Antitumor Immune Memory Impairment Associated With High Tumor Burden and Sensitizes Anti-PD-1 Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting PLD3 Reverses the Immunosuppressive Niche by Reprogramming Tumor-Associated Macrophages and Potentiates Antitumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The weight of the enemy: Tumor burden as a tumor-agnostic prognostic marker and the limits of immunotherapy.Cancer · 2026Article
- Sterol regulatory element‑binding proteins: Master regulators of lipid metabolic reprogramming in cancer and emerging therapeutic targets (Review).Oncology reports · 2026Review
- Heterogeneity of macrophages in PD-1/PD-L1 inhibitor therapy: a single-cell perspective.Cellular & molecular biology letters · 2026Review
- IGFBP in tumor immunity: a novel target for cancer immunotherapy.Journal of translational medicine · 2026Review
- IGFBP2 promotes immunosuppression by regulating macrophage PD-L1 expression in NEUROD1-high small cell lung cancer.Journal of translational medicine · 2026Article
- Mitofusin-2 suppresses tumor immune escape through EGFR/STAT3-mediated PD-L1 transcription.Cell death & disease · 2026Article
- Targeting hypoxic exosomal IGFBP2 overcomes CD47-mediated immune evasion in glioblastoma.Cell death & disease · 2026Article
- Reshaping the immunosuppressive glioma microenvironment: mechanisms, biomarkers, and emerging immunotherapies.Frontiers in immunology · 2026Review
- Single-Cell Sequencing Reveals the Heterogeneity of Glioma and Identifies IGFBP2 as A Potential Therapeutic Target.Oncology research · 2026Article
- Real-world effectiveness of first-line immunotherapy with or without chemotherapy versus chemotherapy alone in advanced non-small cell lung cancer.Frontiers in immunology · 2026Article
- Crosstalk between tumor-associated macrophages and the B7/CD28 family in immune checkpoint inhibitor-induced immunotherapy.Molecular and cellular biochemistry · 2026Review
- STAT3 signaling in cancer: mechanisms and targeting therapeutic.Frontiers in immunology · 2026Review
- AI-engineered multifunctional nanoplatforms: synergistically bridging precision diagnosis and intelligent therapy in next-generation oncology.Journal of nanobiotechnology · 2025Review
- Impact of Tumor Burden on Immune Checkpoint and Conventional Therapy Responses and Outcomes.Cancer research communications · 2025Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral clinical studies have uncovered a negative correlation between baseline tumor burden and the efficacy of immune checkpoint inhibitor (ICI) treatment. This study aimed to uncover the specific mechanisms underlying the difference in sensitivity to ICI treatment between tumors with high (HTB) and low (LTB) tumor burden.
methodsFor in vivo studies, several mouse models of subcutaneous tumors were established, and transcriptome sequencing, immunohistochemistry, and flow cytometry assays were used to detect the immune status in these subcutaneous tumors. For in vitro experiments, co-culture models, cytokine antibody arrays, western blotting, flow cytometry, and enzyme-linked immunosorbent assays were used to explore the underlying molecular mechanisms
resultsWe found that MC38 or B16 subcutaneous tumors from the HTB group did not show any response to anti-programmed cell death protein-1 (PD-1) therapy. Through flow cytometry assays, we found that the infiltration with CD8
conclusionsThis study suggested that the low efficacy of ICI treatment in HTB tumors is mainly attributed to the intratumoral accumulation of PD-L1
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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.