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Role of Ferroptosis – A Novel Programmed Cell Death in Temozolomide Therapy for Brain Cancer

TEMOZOLOMIDE- Role of Ferroptosis in Brain Cancer

Glioblastoma (GBM) are the most prevalent type of primary malignant brain tumor in adults that can develop in the brain stem, cerebellum, or spinal cord. Temozolomide (TMZ) is an alkylating agent that is used to treat adults with newly diagnosed GBM and resistant anaplastic astrocytoma who have progressed on a nitrosourea and procarbazine-containing therapy regimen. Ferroptosis, a novel form of programmed cell death, plays a crucial role in glioblastoma therapy. Cell membrane damage produced by mechanisms such as intracellular iron build-up, reactive oxygen species (ROS), lipid peroxidation, glutathione peroxidase (GPX) activity failure, and x-catenin (xCT) causes ferroptosis (iron dependent programmed cell death). This blog discusses the molecular mechanisms of ferroptosis, its application, and challenges in the development and treatment of glioblastoma. GBM invasiveness and treatment resistance may increase if ferroptosis is avoided due to changes in glucose, lipid, glutamine, and iron metabolism. Targeting ferroptosis, which involves fatal phospholipid peroxidation due to dysregulated redox homeostasis and cellular metabolism, could be a promising treatment for GBM, as it is essential for tumor cell viability.

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