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Mechanisms of drug resistance in Glioblastoma Multiforme


Glioblastoma multiforme (GBM) is a group of low-grade as well as high-grade brain tumors that originate from the glia;neuroglial cells and are the most common and crucial brain tumor, specially in adults. The main causes are deemed to be associated with: Age, race, pre- existence of low grade brain tumor, which over the time may turn into a higher/more progressive grade, and genetic pre- dispositions(Neurofibromatosis, Tuberous sclerosis,Von Hippel-Lindau disease, Li-Fraumeni syndrome, and Turcot syndrome).Current standard of care includes surgical resection, which is followed by radiation therapy and chemotherapy with agent temozolomide (TMZ). These malignant glioblastomic tumor cells have the ability of intrinsic or acquired resistance to surgical, radiation and chemotherapy. Despite the advancement in the therapeutic area, all tumors recur and have a median survival rate of around 12- 14 months only. [21,23]Temozolomide (TMZ) plays an important role as a chemotherapeutic agent for the treatment of GBM, but the satisfaction rate is not up to the mark. This review article focuses on the role of resistance of Temozolomide in the GBM.

Key words: DNA repair, glioblastoma, temozolomide, O6-methylguanine-DNA methyltransferase, apoptosis, autophagy, resistance, Anticancer Drug, Cancer Therapy, Cell Death, DNA Methylation

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