AI Article Synopsis
- The study focuses on how the CSF-1R and its ligands CSF-1 and IL-34 affect tumor-related macrophages, which contribute to tumor growth and decrease anti-tumor immunity.
- The CSF-1R/CSF-1 pathway also plays a role in PVNS, a benign tumor of the synovial tissue, highlighting the need for better treatments for both advanced tumors and PVNS.
- While targeting CSF-1R with drugs or antibodies has shown some promise in lab settings, real-world results have been limited; however, early clinical trials for PVNS show potential, suggesting that blocking this signaling pathway could lead to effective new immunotherapy strategies.
Article Abstract
Purpose Of Review: Colony-stimulating factor 1 receptor (CSF-1R) and its ligands, CSF-1 and interleukin 34 (IL-34), regulate the function and survival of tumor-associated macrophages, which are involved in tumorigenesis and in the suppression of antitumor immunity. Moreover, the CSF-1R/CSF-1 axis has been implicated in the pathogenesis of pigmented villonodular synovitis (PVNS), a benign tumor of the synovium. As advanced or metastatic malignant solid tumors and relapsed/refractory PVNS remain unresolved therapeutic problems, new approaches are needed to improve the outcome of patients with these conditions.
Recent Findings: In solid tumors, targeting CSF-1R via either small molecules or antibodies has shown interesting results in vitro but limited antitumor activity in vivo. Concerning PVNS, clinical trials assessing CSF-1R inhibitors have revealed promising initial outcomes. Blocking CSF-1/CSF-1R signaling represents a promising immunotherapy approach and several new potential combination therapies for future clinical testing.
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| http://dx.doi.org/10.1007/s11912-017-0634-1 | DOI Listing |
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