ArticleCell reports. Medicine2024
TNFR1 signaling promotes pancreatic tumor growth by limiting dendritic cell number and function.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Necroptosis in pancreatic cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Pooled it
- TNFR1 expression on cancer cells mediates immune escape and an immunosuppressive microenvironment.The Journal of experimental medicine · 2026Article
- Mitochondrial double-stranded RNA fuels pancreatic cancer growth via RIG-I/TLR3 inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Antigen-directed single domain antibody-based TNFR1 agonists elicit preferential killing of HER2-overexpressing cancer cells.iScience · 2026Article
- Construction of a SEMA3 family-based model to predict prognosis and molecular subtypes in pancreatic ductal adenocarcinoma.Discover oncology · 2026Article
- Interruption of cross-communication pathways alters the immune cell signature of pancreatic cancer and decreases tumor growth.Cell communication and signaling : CCS · 2026Article
- PRECOG update: an augmented resource of clinical outcome associations with gene expression for adult, pediatric, and immunotherapy cohorts.Nucleic acids research · 2026Article
- Bibliometric analysis of global research trends in pancreatic cancer immunotherapy.Human vaccines & immunotherapeutics · 2025Article
- A 3D Bioprinted Pancreatic Cancer Model Using Collagen-Gelatin Methacrylamide-Alginate Bioinks to Mimic the Desmoplastic Microenvironment.Biomacromolecules · 2025Article
- Therapeutic targeting of cell death-immune crosstalk in cancer to rewire the tumor immune microenvironment.Molecular cancer · 2025Review
- Deciphering TICRR's oncogenic landscape in pancreatic adenocarcinoma: molecular insights and clinical implications.Discover oncology · 2025Article
- Cross-priming in cancer immunology and immunotherapy.Nature reviews. Cancer · 2025Review
- Exploring TNFR1: from discovery to targeted therapy development.Journal of translational medicine · 2025Review
- Current status, challenges, and integration pathways of biomarker classification systems in graft-versus-host disease: a preliminary exploration.Frontiers in medicine · 2025Review
- Targeting molecular pathways to control immune checkpoint inhibitor toxicities.Trends in immunology · 2025Review
- Dendritic cell-related gene signature in pancreatic cancer stratifies patient subtypes and implicates a KCTD14-TNF signaling axis.Frontiers in immunology · 2025Article
- The role of inflammatory factors in the tumor microenvironment of pancreatic cancer.Frontiers in immunology · 2025Review
- Comprehensive Pan-cancer Analysis Revealed CASP10 As a Promising Biomarker For Diverse Tumor Types.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic adenocarcinoma (PDAC) is one the most intractable cancers, in part due to its highly inflammatory microenvironment and paucity of infiltrating dendritic cells (DCs). Here, we find that genetic ablation or antibody blockade of tumor necrosis factor receptor 1 (TNFR1) enhanced intratumor T cell activation and slowed PDAC growth. While anti-PD-1 checkpoint inhibition alone had little effect, it further enhanced intratumor T cell activation in combination with anti-TNFR1. The major cellular alteration in the tumor microenvironment in the absence of TNFR1 signaling was a large increase in DC number and immunostimulatory phenotype. This may reflect a direct effect on DCs, because TNF induced TNFR1-dependent apoptosis of bone-marrow-derived DCs. The therapeutic response to anti-TNFR1 alone was superior to the combination of DC-activating agonistic anti-CD40 and Flt3 ligand (Flt3L). These observations suggest that targeting TNFR1, perhaps in concert with other strategies that promote DC generation and mobilization, may have therapeutic benefits.
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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.