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Excessive ROS production causes oxidative stress to increase mitochondrial DNA damage, further promotes the activation of oncogenes or the inactivation of anti-oncogenes, which facilitates its tumorigenic signaling pathways and tumor progression

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In a randomized controlled trial of an immediate treatment group and a wait-list control group, two 60 minute group-based classes, which lasted for 12 weeks were held for the treatment group

As a result, mitochondrial function is disrupted