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However, sustained high levels of CORT override these protective responses one by one, favoring pathways leading to injury, such as apoptosis signaling triggered by NRPL3, inadequate synthesis of ROS decomposition, nuclear accumulation of FOXO3a, and sustained activation of the Notch pathway and ERS-IRE1/XBP1 signaling pathway, all contributing to cell death

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As temozolomide is widely administered to patients with IDH1-mutant gliomas, Subramani and colleagues [116] used 1 H MRS and hyperpolarized 13 C MRS to identify increased Glu production as a potential metabolic biomarker of temozolomide response in genetically engineered and patient-derived models: in temozolomide-treated cells a significant increase in Glu and 13 C-Glu levels was observed