Figure 4.

Established Heterocellular Signaling In Colorectal Cancer (CRC). Known heterocellular interactions that drive emergent phenotypes in CRC. While much progress has been made, our understanding of heterocellular signaling in cancer is vastly incomplete. For example, in CRC, epithelial–lymphoid and myeloid–stromal interactions are poorly characterized. Moreover, how oncogenic mutations in epithelial cells (e.g., loss of APC, KRAS^G12D, loss of p53) regulate these heterocellular signaling pathways is currently unknown. Abbreviations: AR, amphiregulin; CCL, chemokine (C-C motif) ligand; FGF, fibroblast growth factor; HGF, hepatocyte growth factor; IL, interleukin; SIRP, signal regulatory protein; SHH, Sonic hedgehog; TGF, transforming growth factor.