This 2015 study revealed that high-dose vitamin C selectively induces cytotoxicity in colorectal cancer (CRC) cells with KRAS or BRAF mutations by targeting the glycolytic enzyme GAPDH. The mechanism involves enhanced uptake of dehydroascorbate (DHA) via GLUT1 transporters, followed by intracellular reduction to vitamin C, which consumes glutathione and leads
This study evaluated the effectiveness of plasma-based assays detecting BRAF and NRAS mutations in circulating tumor DNA (ctDNA) for monitoring metastatic melanoma. Involving patients with unresectable stage IIIC/IV melanoma undergoing BRAF inhibitor therapy or immune checkpoint blockade, ctDNA levels were measured using droplet digital PCR. The assays demonstrated higher sensitivity
This 2018 review underscores the critical role of molecular testing for BRAF mutations, particularly the V600E variant, in guiding treatment strategies for advanced melanoma. Approximately 50% of advanced melanomas harbor BRAF mutations, making them amenable to targeted therapies with BRAF and MEK inhibitors, which have demonstrated significant long-term benefits. The
This 2015 news article in Science discusses findings from a study by Yun et al., which demonstrated that high-dose vitamin C selectively kills colorectal cancer cells harboring KRAS or BRAF mutations. The mechanism involves vitamin C entering cancer cells as dehydroascorbic acid (DHA) via GLUT1 transporters. Inside the cell, DHA
