DACH1 and neoplasm: We also demonstrate that the transcription factor and putative tumor suppressor DACH1 (a downstream target of FGF2) is significantly downregulated by lung-derived soluble factors secreted in the presence of primary TNBC tumor, and that inhibition of DACH1 through siRNA or FGF2 treatment increases acquisition of a stem-like ALDHhiCD44+ breast cancer phenotype.