[HTML][HTML] Tumor-induced myeloid deviation: when myeloid-derived suppressor cells meet tumor-associated macrophages

S Ugel, F De Sanctis, S Mandruzzato… - The Journal of clinical …, 2015 - Am Soc Clin Investig
S Ugel, F De Sanctis, S Mandruzzato, V Bronte
The Journal of clinical investigation, 2015Am Soc Clin Investig
The generation of an inflammatory environment is favorable and often decisive for the
growth of both primary tumors and metastases. Tumor cells either express membrane
molecules or release tumor-derived soluble factors able to alter myelopoiesis. Tumor-
reprogrammed myeloid cells not only create a tolerogenic environment by blocking T cell
functions and proliferation, but also directly drive tumor growth by promoting cancer
stemness, angiogenesis, stroma deposition, epithelial-to-mesenchymal transition, and …
The generation of an inflammatory environment is favorable and often decisive for the growth of both primary tumors and metastases. Tumor cells either express membrane molecules or release tumor-derived soluble factors able to alter myelopoiesis. Tumor-reprogrammed myeloid cells not only create a tolerogenic environment by blocking T cell functions and proliferation, but also directly drive tumor growth by promoting cancer stemness, angiogenesis, stroma deposition, epithelial-to-mesenchymal transition, and metastasis formation. In this Review, we discuss the interplay between immunosuppressive and protumoral myeloid cells and detail their immune-regulatory mechanisms, the molecular pathways involved in their differentiation, as well as their potential role as prognostic and diagnostic biomarkers and prospective targets for innovative approaches to treat tumor-bearing hosts.
The Journal of Clinical Investigation