ReviewCancers2017
Promotion of Tumor Invasion by Tumor-Associated Macrophages: The Role of CSF-1-Activated Phosphatidylinositol 3 Kinase and Src Family Kinase Motility Signaling.
Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- Innovative immunotherapeutic strategies for thyroid cancer: challenges and opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Scalable cell-specific coexpression networks for granular regulatory pattern discovery with NeighbourNet.Genome research · 2026Article
- Role of Colony Stimulating Factor 1 (CSF-1) and Its Receptor CSF1R: Macrophage Repolarization for Glioblastoma Treatment.ACS pharmacology & translational science · 2025Review
- JMC14: a novel dual PI3Kδ/CSF1R inhibitor with potent antitumor activity in hematological and solid tumors.Acta pharmacologica Sinica · 2025Article
- P2 purinergic receptor expression and function in tumor-related immune cells.Purinergic signalling · 2025Review
- Insights into CSF-1R Expression in the Tumor Microenvironment.Biomedicines · 2024Review
- The role of tumor-associated macrophages in tumor immune evasion.Journal of cancer research and clinical oncology · 2024Review
- Immunologic tumor microenvironment modulators for turning cold tumors hot.Cancer communications (London, England) · 2024Review
- NF-κB: Governing Macrophages in Cancer.Genes · 2024Review
- The role of macrophage migratory behavior in development, homeostasis and tumor invasion.Frontiers in immunology · 2024Review
- p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression.Cancer discovery · 2023Article
- Challenges and prospects of CSF1R targeting for advanced malignancies.American journal of cancer research · 2023Article
- Effects of the interactions between platelets with other cells in tumor growth and progression.Frontiers in immunology · 2023Review
- Fashionable, but What is Their Real Clinical Usefulness? NLR, LMR, and PLR as a Promising Indicator in Colorectal Cancer Prognosis: A Systematic Review.Journal of inflammation research · 2023Review
- Differential gene expression of immunity and inflammation genes in colorectal cancer using targeted RNA sequencing.Frontiers in oncology · 2023Article
- EMT and Tumor Turning Point Analysis in 3D Spheroid Culture of HNSCC and Mesenchymal Stem Cells.Biomedicines · 2022Article
- Macrophage-Colony-Stimulating Factor Receptor Enhances Prostate Cancer Cell Growth and Aggressiveness In Vitro and In Vivo and Increases Osteopontin Expression.International journal of molecular sciences · 2022Article
- Protein Kinase Inhibitors as a New Target for Immune System Modulation and Brain Cancer Management.International journal of molecular sciences · 2022Review
- Enhancing therapeutic anti-cancer responses by combining immune checkpoint and tyrosine kinase inhibition.Molecular cancer · 2022Review
- Single-cell transcriptomics reveals shared immunosuppressive landscapes of mouse and human neuroblastoma.Journal for immunotherapy of cancer · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages interact with cells in every organ to facilitate tissue development, function and repair. However, the close interaction between macrophages and parenchymal cells can be subverted in disease, particularly cancer. Motility is an essential capacity for macrophages to be able to carry out their various roles. In cancers, the macrophage's interstitial migratory ability is frequently co-opted by tumor cells to enable escape from the primary tumor and metastatic spread. Macrophage accumulation within and movement through a tumor is often stimulated by tumor cell production of the mononuclear phagocytic growth factor, colony-stimulating factor-1 (CSF-1). CSF-1 also regulates macrophage survival, proliferation and differentiation, and its many effects are transduced by its receptor, the CSF-1R, via phosphotyrosine motif-activated signals. Mutational analysis of CSF-1R signaling indicates that the major mediators of CSF-1-induced motility are phosphatidyl-inositol-3 kinase (PI3K) and one or more Src family kinase (SFK), which activate signals to adhesion, actin polymerization, polarization and, ultimately, migration and invasion in macrophages. The macrophage transcriptome, including that of the motility machinery, is very complex and highly responsive to the environment, with selective expression of proteins and splice variants rarely found in other cell types. Thus, their unique motility machinery can be specifically targeted to block macrophage migration, and thereby, inhibit tumor invasion and metastasis.
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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.