In this context CSF1R, the cellular receptor for colony stimulating factor-1 (CSF1) and interleukin 34 (IL-34), occupies a central role in manipulating the behavior of TAMs and the dysregulation of CSF1R signaling has been implicated in cancer progression and immu-nosuppression in many specific cancers.
In ovarian cancers, we show that GAPDH expression is regulated, and we now recognize that one of the many functions of GAPDH is to promote mRNA stability of CSF-1, an important cytokine in tumor progression.
This review aims to summarize recent findings on the role of CSF-1 and its receptor in normal and neoplastic mammary development that may elucidate potential relationships of growth factor-induced biological changes in the breast during pregnancy and tumor progression.
In addition, soluble CSF-1 secreted from the tumor acts to divert antitumor macrophage responses and suppresses the differentiation of mature tumor-antigen-presenting dendritic cell This review discusses these observations in detail and attempts to fit them into a larger picture of CSF-1 and macrophage action in the regulation of normal mammary gland development and tumor progression.
In v-myc-transformed myelomonocytic cells, secondary events occur, such as the expression of colony stimulating factor-1 (CSF-1) which play a critical role in immortalization and subsequent tumor progression.