The colony-stimulating factor-1 receptor (CSF-1R) is known as macrophage colony-stimulating factor receptor (M-CSFR) or CD115. CSF1 receptor (CSF1R)-mediated signaling is crucial for the differentiation and survival of the mononuclear phagocyte system and macrophages in particular. CSF1R belongs to the type III protein tyrosine kinase receptor family, and binding of CSF1 or the more recently identified ligand, IL-34, induces homodimerization of the receptor and subsequent activation of receptor signaling. As the intratumoral presence of CSF1R+ macrophages correlates with poor survival in various tumor types, targeting CSF1R signaling in tumor-promoting TAM represents an attractive strategy to eliminate or repolarize these cells. CSF1R expression can be detected on other myeloid cells within the tumor microenvironment such as dendritic cells, neutrophils, and myeloid-derived suppressor cells (MDSCs). Expression of CSF-1 and/or CSF-1R has been documented in several human malignancies including breast, cervical, endometrial, ovarian, lung, prostate and kidney cancer, as well as in classical Hodgkin’s lymphoma (cHL) and anaplastic large cell lymphoma (ALCL).


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