Abstract

Glioblastoma (GBM) is the most aggressive tumor of CNS characterized by a poor prognosis mainly due to the resistance to the available treatments. Temozolomide (TMZ) is the gold standard for GBM treatment although this drug even in association with radiotherapy provides a median survival of 14.6 months. There are evidences that the increase in intracellular ROS is able to sustain gliomagenesis, tumor proliferation rate, and resistance to treatments by supporting proliferative pathways and metabolism as well as by generating genetic instability causing the establishment of protumorigenic mutants. At the same time, an increase in intracellular ROS, being involved in the oxidative damage of DNA, lipids, and proteins, is involved in the impairment of cell function, triggering also cell death.

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