Abstract
Melanoma is the most life-threatening skin cancer, accounting for 75% of skin cancer-associated death. Vemurafenib was approved by FDA for the treatment of late-stage melanoma patients with BRAF mutation. However, clinically, most cases developed resistance to it. Hereby we conduct a study to explore the possible role of a stress responsive protein, Sestrin2, in vemurafenib resistance. Previously, we have demonstrated Sestrin2 has a protective role in melanoma cells in response to anoikis via detoxifying intracellular reactive oxygen species (ROS).
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