ArticleCancer research2014
CSF1/CSF1R blockade reprograms tumor-infiltrating macrophages and improves response to T-cell checkpoint immunotherapy in pancreatic cancer models.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04663126 (Pilot Study to Test the Feasibility of IV Injected Tc-99m-tilmanocept for Imaging of M2-like Tumour Associated Macrophages in Metastatic Melanoma), which is not on this map. Cited by 872 papers, 1 of them a synthesis that pooled it.
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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.
Pilot Study to Test the Feasibility of IV Injected Tc-99m-tilmanocept for Imaging of M2-like Tumour Associated Macrophages in Metastatic Melanoma
Who cites it
872 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,264 citations in OpenAlex.
- Hyperprogressive disease in carcinoma induced by immune checkpoint inhibitor therapy: a systematic review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Pooled it
- Ad-SGE-DKK3 Gene Therapy Overcomes Resistance to Immune Checkpoint Blockade in Pleural Mesothelioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- Neoadjuvant vidutolimod and nivolumab in high-risk resectable melanoma: A prospective phase II trial.Cancer cell · 2024Trial
- Immune cell clustering identifies a CD163⁺/CSF1R⁺ macrophage and neutrophil-enriched phenotype with distinct biological signatures and poor prognosis in angiosarcoma.Oncoimmunology · 2026Article
- Local delivery of SBRT and IL-12 to murine PDAC tumors modulates hematopoiesis.Oncoimmunology · 2026Article
- Skeletal Muscle Index, Tumor and Systemic Immunity, and Survival in Advanced Pancreatic Ductal Adenocarcinoma.Cancer medicine · 2026Article
- Review
- Secreted protein circuits in the gastrointestinal tumour microenvironment: determinants of immunotherapy response and resistance.Journal of translational medicine · 2026Review
- Review
- Next-generation macrophage engineering in cancer therapy: From TAM reprogramming to CAR-macrophages.Molecular therapy. Nucleic acids · 2026Review
- A pancreatic cancer organoid-macrophage co-culture using starPEG-heparin hydrogel deciphers tumor-immune cell interactions.NPJ precision oncology · 2026Article
- Photothermal-driven sequential immunotherapy overcomes resistance to PARP inhibition inActa pharmaceutica Sinica. B · 2026Article
- Reduced colony-stimulating factor 1 receptor expression in myeloid cells has limited impact on chronic lymphocytic leukaemia progression.British journal of haematology · 2026Article
- Tumor cell-intrinsic NSUN2 deficiency reprograms macrophages to sensitize non-small cell lung cancer to EGFR inhibitors by reversing immune evasion.Neoplasia (New York, N.Y.) · 2026Article
- Pathway-driven therapeutic stratification in pancreatic ductal adenocarcinoma.Translational oncology · 2026Review
- Targeting CCR1 Remodels the Tumor Microenvironment and Relieves Immunosuppression in Pancreatic Cancer.Cancer immunology research · 2026Article
- Targeted Photo-Induced Elimination of Tumor-Associated Macrophages Suppresses Cancer Progression in a Murine Model.Cancer science · 2026Article
- Macrophage Plasticity in Cancer Therapy: Function, Timing, and Tradeoffs.International journal of molecular sciences · 2026Review
- Unravelling the pathogenesis and therapeutic approaches of pancreatic ductal adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Ecosystem-matched reprogramming of the tumor-immune microenvironment to overcome cancer immunotherapy resistance.Molecular cancer · 2026Review
812 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Cancer immunotherapy generally offers limited clinical benefit without coordinated strategies to mitigate the immunosuppressive nature of the tumor microenvironment. Critical drivers of immune escape in the tumor microenvironment include tumor-associated macrophages and myeloid-derived suppressor cells, which not only mediate immune suppression, but also promote metastatic dissemination and impart resistance to cytotoxic therapies. Thus, strategies to ablate the effects of these myeloid cell populations may offer great therapeutic potential. In this report, we demonstrate in a mouse model of pancreatic ductal adenocarcinoma (PDAC) that inhibiting signaling by the myeloid growth factor receptor CSF1R can functionally reprogram macrophage responses that enhance antigen presentation and productive antitumor T-cell responses. Investigations of this response revealed that CSF1R blockade also upregulated T-cell checkpoint molecules, including PDL1 and CTLA4, thereby restraining beneficial therapeutic effects. We found that PD1 and CTLA4 antagonists showed limited efficacy as single agents to restrain PDAC growth, but that combining these agents with CSF1R blockade potently elicited tumor regressions, even in larger established tumors. Taken together, our findings provide a rationale to reprogram immunosuppressive myeloid cell populations in the tumor microenvironment under conditions that can significantly empower the therapeutic effects of checkpoint-based immunotherapeutics.
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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.