Abstract
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.
Authors
Stefano Ugel, Francesco De Sanctis, Susanna Mandruzzato, Vincenzo Bronte
Figure 1
Common phenotypic markers of MDSCs and TAMs.
Several phenotypic markers of mouse and human MDSCs (
Copyright © 2017 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)