ArticleThe Journal of experimental medicine2023
Stromal and therapy-induced macrophage proliferation promotes PDAC progression and susceptibility to innate immunotherapy.
Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 40 citations in OpenAlex.
- Biomarkers of response to neoadjuvant palbociclib plus anastrozole in endocrine-resistant estrogen receptor-positive/HER2-negative breast cancer: a phase 2 trial.Nature communications · 2026Trial
- Quiescent tumor cells shape the immunosuppressive microenvironment in pancreatic cancer.Nature communications · 2026Article
- CD40 Agonism in Pancreatic Ductal Adenocarcinoma: Expression, Biology, and Therapeutic Targeting.Cancers · 2026Review
- High-Dimensional Protein Analysis Uncovers Distinct Immunologic and Stromal Features in Primary and Metastatic Pancreatic Ductal Adenocarcinoma.Cancer research · 2026Article
- Therapeutic reprogramming of tumour-associated macrophages in pancreatic cancer using a cytotoxic CCR2-targeted nanotheranostic.Molecular cancer · 2026Article
- CD4+ T Cells Mediate MHC-Deficient Tumor Rejection and Endothelial Cell Reprogramming.Cancer immunology research · 2026Article
- KRAS-driven cytokine-metabolic crosstalk shapes immune exclusion in pancreatic ductal adenocarcinoma.Frontiers in genetics · 2026Review
- Review
- Nanotechnology-enhanced immunotherapies for pancreatic ductal adenocarcinoma: challenges and opportunities.Drug delivery and translational research · 2025Review
- Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis.Cancer research communications · 2025Article
- Understanding the complexity of tumor-associated macrophages: Druggable and therapeutic insights.Acta pharmaceutica Sinica. B · 2025Review
- Importance of landscape exploration and progress in molecular therapies and precision medicine for pancreatic ductal adenocarcinoma.World journal of gastrointestinal oncology · 2025Review
- Review
- Depletion of tumor-derived CXCL5 improves T cell infiltration and anti-PD-1 therapy response in an obese model of pancreatic cancer.Journal for immunotherapy of cancer · 2025Article
- Emerging macrophage-based therapies for cancer: a review of preclinical and clinical advances.Frontiers in immunology · 2025Review
- Unveiling the resistance to therapies in pancreatic ductal adenocarcinoma.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024Review
- Metabolic landscape of the healthy pancreas and pancreatic tumor microenvironment.JCI insight · 2024Article
- FAM53B promotes pancreatic ductal adenocarcinoma metastasis by regulating macrophage M2 polarization.World journal of gastrointestinal oncology · 2024Article
- GPER1 signaling restricts macrophage proliferation and accumulation in human hepatocellular carcinoma.Frontiers in immunology · 2024Article
- Characterization of cancer-associated fibroblasts (CAFs) and development of a CAF-based risk model for triple-negative breast cancer.Cancer cell international · 2023Article
Corrections and comments
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Authors and funding
21 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor-associated macrophages (TAMs) are abundant in pancreatic ductal adenocarcinomas (PDACs). While TAMs are known to proliferate in cancer tissues, the impact of this on macrophage phenotype and disease progression is poorly understood. We showed that in PDAC, proliferation of TAMs could be driven by colony stimulating factor-1 (CSF1) produced by cancer-associated fibroblasts. CSF1 induced high levels of p21 in macrophages, which regulated both TAM proliferation and phenotype. TAMs in human and mouse PDACs with high levels of p21 had more inflammatory and immunosuppressive phenotypes. p21 expression in TAMs was induced by both stromal interaction and/or chemotherapy treatment. Finally, by modeling p21 expression levels in TAMs, we found that p21-driven macrophage immunosuppression in vivo drove tumor progression. Serendipitously, the same p21-driven pathways that drive tumor progression also drove response to CD40 agonist. These data suggest that stromal or therapy-induced regulation of cell cycle machinery can regulate both macrophage-mediated immune suppression and susceptibility to innate immunotherapy.
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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.