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We recently linked hyperactivation of Nrf2 through both mutational and transcriptional mechanisms to acquisition and maintenance of resistance to chemotherapy and radiation, the two mainstay treatments for HNSCC as well as for many other solid tumors [18, 19, 51]

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The result: defective bacterial clearance, the researchers reported in February in PLOS ONE

Although the detailed mechanism remains unclear, this study suggests that the combination of ACR, MVK and CPO exerts additive or synergistic effects on proinflammatory cytokine expression through ROS production and mtDNA release in HUVECs