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Thus, we have demonstrated that GSH-targeted therapy selectively kills PC cells in an oxidative stress-dependent manner and that the differences in basal ROS level and antioxidant scavenging capacity induced by stratified expression of VRK2 can well account for the heterogeneous sensitivity to GSH inhibition
Understanding the metabolic mechanisms underlying breast cancer metastasis will provide important clues to develop novel therapeutic approaches for treatment of metastatic breast cancer
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Kaltsas A, Hatzichristou D
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