Reverse transcriptase inhibition potentiates target therapy in BRAF-mutant melanomas. effects on cell proliferation, apoptosis, DNA-damage, ROS induction and mitochondrial membrane depolarization
Target therapies based on BRAF and MEK inhibitors (MAPKi) have changed the therapeutic landscape for metastatic melanoma patients bearing mutations in the BRAF kinase. However, the emergence of drug resistance imposes the necessity to conceive novel therapeutic strategies capable to achieve a more durable disease control. In the last years, retrotransposons laying in human genome have been shown to undergo activation during tumorigenesis, where they contribute to genomic instability.