CSF-1/CSF-1R targeting agents in clinical development for cancer therapy.
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Summary
The currently available information on efficacy and safety of various CSF-1/CSF- 1R inhibitors in cancer patients is discussed and potential combination partners emerging from preclinical studies are highlighted while considering the differences between mouse and human macrophage biology.
- Type
- review
- Published
- 2015-08-01
- Cited by
- 130
- References
- 55
- OpenAlex
- https://openalex.org/W642285930
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:206974576
Keywords
Blockade, Cancer, Innate immune system, Cancer therapy, Macrophage
References
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Cited by
- Functions of interleukin‐34 and its emerging association with rheumatoid arthritis
- Reprogramming of macrophages--new opportunities for therapeutic targeting.
- Dissecting the Multiple Myeloma-bone microenvironment reveals new therapeutic opportunities
- SCS macrophages suppress melanoma by restricting tumor-derived vesicle–B cell interactions
- Timing of CSF-1/CSF-1R signaling blockade is critical to improving responses to CTLA-4 based immunotherapy
- Prioritization schema for immunotherapy clinical trials in glioblastoma
- Radiation effects on the tumor microenvironment: Implications for nanomedicine delivery☆
- Suppression of microRNA activity amplifies IFN-γ-induced macrophage activation and promotes anti-tumour immunity
- Biological role of granulocyte macrophage colony‐stimulating factor (GM‐CSF) and macrophage colony‐stimulating factor (M‐CSF) on cells of the myeloid lineage
- Macrophage Susceptibility to Emactuzumab (RG7155) Treatment
- Development of a RSK Inhibitor as a Novel Therapy for Triple Negative Breast Cancer
- Colony-stimulating factor 1 receptor blockade prevents fractionated whole-brain irradiation-induced memory deficits
- B cells and macrophages pursue a common path toward the development and progression of chronic lymphocytic leukemia
- High Potency VEGFRs/MET/FMS Triple Blockade by TAS-115 Concomitantly Suppresses Tumor Progression and Bone Destruction in Tumor-Induced Bone Disease Model with Lung Carcinoma Cells
- mTORC2-IRF4 mediated metabolic reprograming is essential for macrophage alternative activation
- Innate immune mediators in cancer: between defense and resistance
- Molecular Pathways: Deciphering Mechanisms of Resistance to Macrophage-Targeted Therapies
- Origins of Brain Tumor Macrophages.
- CS2164, a novel multi‐target inhibitor against tumor angiogenesis, mitosis and chronic inflammation with anti‐tumor potency
- Beyond checkpoint inhibition – Immunotherapeutical strategies in combination with radiation
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