Pulmonary reactions to novel chemotherapeutic agents and biomolecules
Philippe Camus, Edward C Rosenow in Drug-induced and Iatrogenic Respiratory Disease, 2010
Clinical experience with macrophage colony-stimulating factor (M-CSF, also called CSF-1) is fairly limited, as its specificity for cells of the monocyte lineage has prevented broad clinical utility.48 Few studies have commented on potential pulmonary side-effects. Zamkoff and colleagues administered a range of M-CSF dosages to 20 patients with advanced malignancies and reported acute dyspnoea in three subjects.49 The investigators felt that the dyspnoea was related to the rate of M-CSF infusion. Another phase I trial of 36 patients with cancer documented one patient with chronic obstructive pulmonary disease who experienced dyspnoea and oxygen desaturation at the highest dose of M-CSF in combination with IFN-γ.50 Most other studies on M-CSF have shown no pulmonary toxicity.
Synovial Fluid
Verna Wright, Eric L. Radin in Mechanics of Human Joints, 2020
Cytokines have been identified in SF. However, their cellular origins often remain speculative. Also, their physiological role in the inflammed joint remains uncertain because of their multiple functions and target cells. A tentative functional classification was suggested by Harris. Interleukin-2, interleukin-3, interleukin-4, and interferon-γ are produced by Tlymphocytes, and their functions relate to activation and amplification of cellular and humoral immune responses. Interleukin-1, interleukin-6, colony-stimulating factor 1, and tumor necrosis factor a originate from macrophages-fibroblasts, and they have broad effects on cells, resulting in proliferation, increased prostaglandin formation, protease activity, bone resorption, and fever. Interestingly, cytokines originating from lymphocytes seem to be low in SF, whereas those from macrophages-fibroblasts are high. The hypothesis has been that macrophage-fibroblast originating substances inhibit lymphocyte cytokines, at least in rheumatoid joints (52).
Dissemination and adhesion of peritoneal cancer cells to the peritoneal wall
Wim P. Ceelen, Edward A. Levine in Intraperitoneal Cancer Therapy, 2015
CAFs are not the only cells in the tumor stroma that influence cancer cells. Tumor-associated macrophages (TAMs) play an important role in the tumor stroma. Ovarian cancer cells express monocyte chemoattractant protein-1 (MCP-1) and macrophage colony-stimulating factor to recruit monocytes and differentiate them into macrophages. IL-10, an TGF-β2 from ovarian cancer cells, can activate the macrophages to become TAMs. MCP-1 is also secreted by TAMs and CAFs creating an auto- and paracrine loop sustaining the TAM activation. TAMs produce, just like CAFs, MMPs helping the cancer cells to invade into the tumor stroma and are therefore associated with poor outcome for cancer patients [48]. Cancer cells and CAFs recruit and differentiate endothelial progenitors to endothelial cells by the secretion of SDF-1. The endothelial cells form new blood vessels stimulated by IL-6 and VEGF-A from CAFs. Angiogenesis supplies the newly formed metastases with oxygen and nutrition allowing them to grow. This is further aided by adipocytes via secretion of leptin and the transfer of lipids [48].
MEOX2 serves as a novel biomarker associated with macrophage infiltration in oesophageal squamous cell carcinoma and other digestive system carcinomas
Published in Autoimmunity, 2021
Zhen Wang, Han Yang, Rusi Zhang, Bin Luo, Bingchen Xu, Zhihua Zhu, Peng Lin
Colony-stimulating factor 1 (CSF-1) is essential for the proliferation and differentiation of macrophages. Thus, we explored correlations between the mRNA expression of MEOX2 and the mRNA expression of colony-stimulating factor 1 (CSF-1) and colony-stimulating factor 1 receptor (CSF-1R) with the TIMER database. The results showed that MEOX2 expression exhibited positive correlations with the mRNA expression of CSF-1 (r = 0.336, p = 2.84e-6) and CSF-1R (r = 0.475, p = 8.07e-12) in oesophageal carcinoma. Further analysis indicated that in the other digestive system carcinomas, MEOX2 expression exhibited positive correlations with the mRNA expression of CSF-1 and CSF-1R, and the correlations in these kinds of carcinomas were even more obvious (Table 2, Figure 7).
Current and emerging systemic therapies for cutaneous metastatic melanoma
Published in Expert Opinion on Pharmacotherapy, 2019
Robert Mason, Lewis Au, Alvaro Ingles Garces, James Larkin
Colony-stimulating factor 1 receptor (CSF1R) is a membrane protein receptor for colony stimulating factor 1, which alters macrophage production and function. It is often overexpressed on tumor infiltrating macrophages. CSF1R-mediated signaling promotes differentiation and survival of macrophages, and binding of CSF1 induces homodimerization of the receptor and subsequent activation. The presence of CSF1R expressing macrophages in tumors has been found to correlate with worse survival outcomes. Multiple CSF1R inhibitors are in development (Pexidartinib, PLX7486, ARRY-382, JNJ-40346527, BLZ945, Emactuzumab, AMG820, IMC-CS4) and several have entered early phase clinical trials alone and in combination with ICI, in solid tumors, melanoma and specifically C-Kit mutant melanoma.
Dysregulated metabolism: A friend-to-foe skewer of macrophages
Published in International Reviews of Immunology, 2023
Keywan Mortezaee, Jamal Majidpoor
Colony stimulating factor-1 (GSF-1) (also called macrophage-colony stimulating factor (M-CSF) interacts with CSF-1R for regulation of macrophage differentiation, survival and migration. CSF-1R is belonged to the receptor protein tyrosine kinase that is contributed to the induction of many types of proto-oncogenes [8]. Autocrine consumption of CSF-1 by differentiating MΦ cells is augmented under lactate exposure. In fact, under lactate exposure, expression of CD163 in macrophages is reinforced by CSF-1 and IL-6, indicating their contribution to the acquisition of M2-like phenotype in macrophages [69]. CSF-1 is highly presented in PDAC. CSF-1 inhibitors reduce the number of CD206 high TAMs in murine PDAC. Presence of CD206 high TAMs in human counterpart is associated with the poor clinical outcomes [104]. CSF-1R blockade in mouse model of breast cancer stimulates an inflamed type I IFN response and augments the efficacy of platinum-based chemotherapy [105]. CSF-1 is also released from GBM cells and turns macrophages into ‘bad macrophages’, while administration of the CSF-1R inhibitor BLZ945 mitigates tumor-promoting TAMs [106] and suppresses tumor progression [107].
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