ArticleCell reports. Medicine2025
Targeting CTGF overcomes resistance to CSF1R inhibitors by preventing CAF activation in colorectal cancer.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Immune cell clustering identifies a CD163⁺/CSF1R⁺ macrophage and neutrophil-enriched phenotype with distinct biological signatures and poor prognosis in angiosarcoma.Oncoimmunology · 2026Article
- CTGF: The remodeler of the tumor immune microenvironment (Review).Oncology reports · 2026Review
- Anoikis in cancer: molecular mechanisms, resistance, and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- Microenvironment-Driven Reprogramming in Colorectal Cancer Liver Metastasis: Metabolic, Phenotypic, and Immune Adaptation.International journal of molecular sciences · 2026Review
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- Cancer-associated fibroblasts and tertiary lymphoid structure orchestrate the spatial architecture of tumor immunity.Journal of hematology & oncology · 2026Review
- Cancer-Associated Fibroblasts in Gastrointestinal Cancer Metastasis: Mechanisms and Emerging Therapeutic Strategies.Drug design, development and therapy · 2026Review
- The MAPK Pathway Coordinates an Immunosuppressive Microenvironment in Colorectal Cancer: A Single-Cell Guided Prognostic Model.Cancer informatics · 2026Article
- Integrative single-cell and bulk RNA-seq analysis identifies glycosyltransferases-related signature in triple negative breast cancer.Functional & integrative genomics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting the colony-stimulating factor 1 receptor (CSF1R) pathway to deplete tumor-associated macrophages (TAMs) represents a promising strategy to overcome immunotherapy resistance in colorectal cancer (CRC). However, resistance to CSF1R inhibitors limits effectiveness. We find that CSF1R inhibition, while effectively reducing TAM abundance, fails to suppress tumor growth. Through imaging mass cytometry (IMC), we further reveal that the CSF1R inhibitor PLX3397 indirectly activates cancer-associated fibroblasts (CAFs), impedes T cell infiltration, and suppresses T cell function. Mechanistically, CSF1R inhibitors unexpectedly activate the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway, which promotes connective tissue growth factor (CTGF) release and subsequent CAF activation. Critically, anti-CTGF therapy rescues CSF1R inhibitor efficacy in vivo. The addition of checkpoint immunotherapy to CSF1R inhibitor and anti-CTGF in animal models leads to complete tumor regression. This combination strategy presents a potential approach to enhance the efficacy of immune checkpoint inhibitors in CRC.
Indexed as
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.