The article reviews the role of Colony-Stimulating Factor 1 Receptor (CSF-1R) in cancer, highlighting its expression and function in both myeloid cells and cancer cells. CSF-1R, primarily expressed on monocytes and macrophages, plays a crucial role in monocyte survival and differentiation. Its overexpression is associated with aggressive tumors characterized by an immunosuppressive microenvironment and poor prognosis. Recent studies have shown that CSF-1R is also expressed on the surface of cancer cells, where it supports tumor progression through autocrine signaling. CSF-1R signaling enhances cell transformation, proliferation, invasion, stemness, and drug resistance. The review discusses the mechanisms underlying CSF-1R expression in cancer cells, including genetic mutations and epigenetic alterations. It also covers therapeutic strategies targeting CSF-1R, such as monoclonal antibodies and small-molecule inhibitors, which have shown promise in clinical trials. The authors emphasize the need for further research to understand the precise mechanisms regulating CSF-1R expression in cancer cells and to develop novel therapeutic approaches.The article reviews the role of Colony-Stimulating Factor 1 Receptor (CSF-1R) in cancer, highlighting its expression and function in both myeloid cells and cancer cells. CSF-1R, primarily expressed on monocytes and macrophages, plays a crucial role in monocyte survival and differentiation. Its overexpression is associated with aggressive tumors characterized by an immunosuppressive microenvironment and poor prognosis. Recent studies have shown that CSF-1R is also expressed on the surface of cancer cells, where it supports tumor progression through autocrine signaling. CSF-1R signaling enhances cell transformation, proliferation, invasion, stemness, and drug resistance. The review discusses the mechanisms underlying CSF-1R expression in cancer cells, including genetic mutations and epigenetic alterations. It also covers therapeutic strategies targeting CSF-1R, such as monoclonal antibodies and small-molecule inhibitors, which have shown promise in clinical trials. The authors emphasize the need for further research to understand the precise mechanisms regulating CSF-1R expression in cancer cells and to develop novel therapeutic approaches.