| Literature DB >> 29080702 |
Sabine Hombach-Klonisch1, Maryam Mehrpour2, Shahla Shojaei3, Craig Harlos4, Marshall Pitz4, Ahmed Hamai2, Krzysztof Siemianowicz5, Wirginia Likus6, Emilia Wiechec7, Brian D Toyota8, Reyhane Hoshyar9, Amir Seyfoori10, Zahra Sepehri11, Sudharsana R Ande12, Forough Khadem13, Mohsen Akbari10, Adrienne M Gorman14, Afshin Samali14, Thomas Klonisch15, Saeid Ghavami16.
Abstract
Despite advances in neurosurgical techniques and radio-/chemotherapy, the treatment of brain tumors remains a challenge. This is particularly true for the most frequent and fatal adult brain tumor, glioblastoma (GB). Upon diagnosis, the average survival time of GB patients remains only approximately 15months. The alkylating drug temozolomide (TMZ) is routinely used in brain tumor patients and induces apoptosis, autophagy and unfolded protein response (UPR). Here, we review these cellular mechanisms and their contributions to TMZ chemoresistance in brain tumors, with a particular emphasis on TMZ chemoresistance in glioma stem cells and GB.Entities:
Keywords: Alkylating drugs; Apoptosis; Autophagy; Bcl-2 family protein; Brain tumor; Cancer therapy; Cell death; DNA repair; Glioblastoma; Glioblastoma stem cells; Temozolomide; Unfolded protein response
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Year: 2017 PMID： 29080702 DOI： 10.1016/j.pharmthera.2017.10.017
Source DB: PubMed Journal: Pharmacol Ther ISSN： 0163-7258 Impact factor: 12.310