Table 3.

Pharmacologically-induced CSCC.

Drug	Treatment	Mechanisms to Promote CSCC	Options to Reduce CSCC Risk
Cyclosporine	Immunosuppressant	Reduces UVB-induced DNA damage repair and inhibits apoptosis by inhibiting nuclear factor of activated T-cells (NFAT) [140]	Sirolimus and everolimus [95,96,97,149,150,151,152]
		Induces the expression of ATF3, which downregulates p53 and increases CSCC formation [141]
		Enhances AKT activation by suppressing PTEN and promotes tumor growth [142,143]
		Enhances epithelial-to-mesenchymal transition involving the upregulation of TGFβ signaling [144]
Azathioprine	Immunosuppressant	Photosensitizes the skin to ultraviolet radiation (UVR) by changing the absorption interval of DNA upon incorporation of 6-thioguanine and induces the formation of reactive oxygen species [159,160,161]	Mycophenolate mofetil [146,162,163]
Voriconazole	Antifungal	The primary metabolite, voriconazole N-oxide, absorbs UVA and UVB wavelengths and causes photosensitivity [166,167,168]	Photoprotection
		Inhibits terminal epithelial differentiation pathways resulting in poor formation of epithelial layers that are important for photoprotection [169]
		Inhibits catalase, raising intracellular levels of UV-associated oxidative stress and DNA damage [170]
Vismodegib (Sonic-hedgehog inhibitor)	Basal cell carcinoma	Activates RAS-MAPK pathway [179]	Close follow-up
Vemurafenib and dabrafenib (BRAF inhibitors)	Melanoma	Activate, paradoxically, MAPK pathway and induce RAS mutations [51,190,191,192,197]	BRAF inhibitors + MEK inhibitors [193,194,195,196] or BRAF inhibitors + cyclooxygenase (COX)-2 inhibitors [200,202]