Circulating tumor cells (CTC) shed from primary PDAC tumors interact with myeloid cells in the portal blood and have the potential to sway myeloid differentiation toward immunosuppressive MDSC and tumor supportive myeloid-derived fibroblasts (M-FB) through activation of CSF1R and CXCR2 signaling pathways mediated by M-CSF/IL-34 and IL-8, respectively. Here, CXCR2 is linked to neoplasm.