Answers are grounded in this paper and cite their sources.
Myeloid cells are key elements of the cancer-related inflammation with the potential to support not only tumor growth but also invasion and metastasis. Tumor-derived factors affect myeloid cell differentiation inducing a phenotype that supports tumor growth, inducing immunosuppression, angiogenesis and tissue remodeling. Soluble mediators, produced at primary tumor site, can also act in a remote mode inducing the release from bone marrow of myeloid cells that have immunosuppressive activities in tumor-draining lymphoid organs and can predispose to colonization when migrate to metastatic organs. We will here review current knowledge on the contribution of tumor-derived signals that affect polarized activation of myeloid cells, their bone marrow release and recruitment to metastatic sites with a particular focus on the role of chemokines.
No takes yet. Share an insight, caveat, or question.
Caronni et al. (2014) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: