She examined the inhibitory signaling molecule TGF-β, which is found near the blood vessels of a tumor. Although the effects of TGF-β and how it restrains normal skin cell growth had been studied by researchers before Fuchs, she specifically looked at the intermediate steps of tumor progression by creating a TGF-β reporter system. She accomplished this by developing tumor cells that expressed a gene commonly found in skin cancer cells, HRasD12V.
Her research demonstrated that cancerous stem cells lacking the TGF-β signal proliferate more quickly but are sensitive to antiproliferative drugs. In contrast, cancerous stem cells that received the TGF-β signal proliferated at a slower rate than those lacking the TGF-β signal but were resistant to antiproliferative drugs. She showed the ability of TGF-β to cause up-regulation of the glutathione pathway, which allowed the SCCs to counter the radical oxygen species often used in radiotherapy and chemotherapy.