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- W2163111310 abstract "5 ISSN 2045-0907 10.2217/CNS.13.52 © 2014 Future Medicine Ltd CNS Oncol. (2014) 3(1), 5–7 Glioblastoma (GB) is the most common and most destructive form of primary brain tumor. Currently, the standard treatment for patients with GB consists of surgical resection, radiotherapy and chemotherapy with temozolomide (TMZ). These tumors have been well characterized for their resistance to standard therapeutic strategies and, despite decades of research, the median survival remains less than 15 months [1]. One of the proposed mechanisms for therapeutic resistance in GB is the activation of stressinduced autophagy. Autophagy is a form of self-degradation in which intracellular components are sequestered in double membrane vesicles called autophagosomes, which then fuse with lysosomes, allowing the recycling of cytoplasmic materials. Inhibition of this process is typically carried out using early-stage inhibitors, such as 3-MA and wortmannin, to prevent the initiation and elongation of the phagophore or late-stage inhibitors, such as bafilomycin-A1, chloroquine (CQ) and hydroxychloroquine (HCQ), which target the functionality of the lysosome in fusing and recycling autophagosomes [2]. The role of autophagy in the development of cancer and response to chemotherapy is highly controversial. The allelic loss of BECN1, the mammalian ortholog of yeast Atg6, results in a high incidence of spontaneous tumors in mice, suggesting BECN1 has a tumor suppressor role [3,4]. Autophagy is thought to play a significant role in the removal of damaged/ oncogenic proteins as well as damaged organelles, and mutations in autophagy genes have been associated with numerous cancers [2]. Interestingly, while the induction of autophagic-dependent cell death has been proposed as a mechanism of cytotoxicity for some chemotherapeutics, activation of autophagy in the context of most therapies has been associated with prosurvival signaling through the maintenance of cellular integrity in response to metabolic and hypoxic stress [5,6]. The currently accepted hypothesis for this paradox is that autophagy may suppress tumor initiation, but promote established tumor progression and resistance to therapeutics [2,7]. While numerous cytotoxic therapeutics have been shown to induce autophagosome formation, the consequences seem to" @default.
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- W2163111310 date "2014-01-01" @default.
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- W2163111310 title "How efficient are autophagy inhibitors as treatment for glioblastoma?" @default.
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- W2163111310 doi "https://doi.org/10.2217/cns.13.52" @default.
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