In the original article [...]

Melanoma is known to be a radioresistant cancer. Melanoma radioresistance can be due to several factors such as pigmentation, antioxidant defenses and high Deoxyribonucleic acid (DNA) repair efficacy. However, irradiation induces intracellular translocation of RTKs, including cMet, which regulates response to DNA damage activating proteins and promotes DNA repair. Accordingly, we hypothesized that co-targeting DNA repair (PARP-1) and relevant activated RTKs, c-Met in particular, may radiosensitize wild-type B-Raf …

<div>Abstract<p>Amplification or activating mutations of c-Kit are a frequent oncogenic alteration, which occurs commonly in acral and mucosal melanoma. Among c-Kit inhibitors, dasatinib is the most active due to its ability to bind both active and inactive conformations of the receptor. However, its use as a single agent in melanoma showed limited clinical benefit. We first found that sensitivity to dasatinib is restricted to melanoma cell lines harboring c-Kit alteration but, unexpectedly, we observe…

<p>Supplementary Figure Legends 1-4</p>

<p>Figure S1. Effect of dasatinib on melanoma cells. Figure S2. CRTC3/MITF/Bcl-2 activation conferred resistance to dasatinib in c-Kit/mutant melanoma cells. Figure S3: Knock out of Bcl-2 sensitizes HBL-R to dasatinib. Figure S4: Effects of dasatinib on anti-apototic proteins.</p>