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Monocytes are essential components of the innate immune system responsible for phagocytosis of pathogens, dead cells, and anti-tumor activities. These cells are involved in a remarkably diverse array of homeostatic processes ranging from host defense to tissue turnover and are emerging as key players in the pathophysiology of several diseases including atherosclerosis, arthritis, obesity, autoimmunity, and cancer. These mononuclear blood cells respond to “self” and “non-self” stimulatory signals by mediating immune responses, controlling inflammatory cytokines, and accumulating at sites of “danger”. Thus, monocytes play a critical role in the protection against invaders. In the case of invader “tumors”, monocyte accumulation has been shown to promote neoangiogenesis and tumor progression. This paradoxical role of monocytes in normal and tumor development may result in the polarized expression of either proor anti-tumor functions. Recognition of diverse monocyte subsets helps explain the plethora of functions attributed to monocytes in acute and chronic inflammatory diseases. Microenvironmental signals, to which monocytes are exposed, play a key role in the setting of their phenotype selectively tuning their functions. In the tumor microenvironment, recruitment of selected monocyte subsets and the inhibition of the apoptotic program promote increase numbers of macrophages in the tumor. A complex network of differentiation factors and inflammatory stimuli determine monocyte life span by blocking the apoptotic pathway and activating a myriad of survival pathways. The present chapter will discuss molecular changes that dictate the fate and behavior of monocyte subsets contributing to tumor biology. In addition, we will discuss the antagonistic and synergistic interplay of transcriptional and posttranscriptional regulatory networks that contribute to the specification of monocytic cell fate and their contribution in tumor progression. The recognition of these molecular networks will furnish strategies to decrease monocytic cell recruitment, survival at the tumor sites, and facilitate monocytic “re-education” programs reestablishing their normal anti-tumor function helping to define novel therapeutic strategy against cancer and other inflammatory diseases.

Monocyte Subsets and Their Role in Tumor Progression