CSF1R and neoplasm: Additionally, an autocrine signaling mechanism has also been described in xenograft models of the claudin-low subtype of breast cancer, where TGF-β-driven CSF-1R expression maintains the claudin-low phenotype but promotes invasive potential by suppressing junctional proteins; inhibition of CSF-1R signaling in the same model leads to the upregulation of luminal cytokeratins with a reduction in tumor cell invasiveness but enhanced proliferative capacity [14].