Potential contribution of tumor‐associated slan + cells as anti‐CSF‐1R targets in human carcinoma

The precise identification of the types and respective roles of the tumor‐associated myeloid cells, which include tumor‐associated Mϕs (TAMs), neutrophils, dendritic cells, and myeloid‐derived suppressor cells, is under intensive investigation. Although tumor‐associated myeloid cells may contribute to tumor cell eradication by virtue of their effector functions, they are retained to fulfill predominantly protumorigenic roles. It follows that depletion of tumor‐associated myeloid cells represents one of the currently pursued therapeutic options in advanced malignancies. In that regard, RG7155/emactuzumab, a specific anti‐CSF‐1R humanized Ab, has been reported recently to deplete CSF‐1R + TAMs, in association with objective clinical responses in patients with advanced cancer. Because RG7155/emactuzumab has also been shown to deplete blood non‐classic CD14 dim/− CD16 ++ monocytes, which in large part include the CD16 ++ slan + monocytes, we asked whether RG7155/emactuzumab could target tumor‐associated slan + cells. In this study, we confirmed that slan + cells localize only to metastatic tumor‐draining lymph nodes, not to primary tumors or distant metastases in patients with different types of carcinoma. Notably, by cell scoring on serial sections, we found that slan + cells represent a minor fraction of the total CSF‐1R + cell pool, suggesting that slan + cells potentially represent minor targets of anti‐CSF‐1R therapy. Therefore, a protumorigenic role for slan + cells, such as that of CSF‐1R + TAMs, based on our current data, remains questionable.