February 25, 2019—Solar UV irradiation of the skin causes DNA damage that. if not repaired correctly, can cause mutations. This is why cutaneous melanoma cells often have a high mutational burden, making the cancer more aggressive and difficult to treat. However, it is not known whether these cells have specific pro-survival mechanisms or enhanced DNA repair capacity. In this article published in Genes and Development (PDF), Katie Herbert and colleagues from Colin Goding’s lab show that BRN2—a transcription factor that drives invasiveness and regulates cell proliferation in melanoma—associates with sites of DNA damage and promotes a more error-prone DNA repair mechanism. BRN2, they find, also reduces cell death of damaged cells. This work has implications for the treatment of melanoma using DNA-damaging agents in cancers expressing BRN2.