Abstract
Glioma stem-like cells (GSCs) were first described as a population which may in part be resistant to traditional chemotherapeutic therapies and responsible for tumour regrowth. Knowledge of the underlying metabolic complexity governing GSC growth and function may point to potential differences between GSCs and the tumour bulk which could be harnessed clinically. There is an increasing interest in the direct/indirect targeting or reprogramming of GSC metabolism as a potential novel therapeutic approach in the adjuvant or recurrent setting to help overcome resistance which may be mediated by GSCs. In this review we will discuss stem-like models, interaction between metabolism and GSCs, and potential current and future strategies for overcoming GSC resistance.
Highlights
Innovative treatment approaches to Glioblastoma (GBM) have far been unsuccessful in part due to therapeutic resistance, resulting in disease recurrence [1]
The objective of this review is to investigate experimental evidence for Glioma stem-like cells (GSCs) metabolic flexibility and bioenergetic capacity in comparison with normal and tumour bulk cells
Due to the pressing need for increasing GBM survival beyond such dismal figures, this review aims to give an overview of the rationale behind new metabolic strategies for GBM treatment, with a focus on the GSC population
Summary
Innovative treatment approaches to Glioblastoma (GBM) have far been unsuccessful in part due to therapeutic resistance, resulting in disease recurrence [1]. GBM is the most common intrinsic brain tumour in adults and is classed as the highest grade (IV) astrocytoma by the World Health Organisation (WHO) [2]. GBMs have been categorised based on whether they derive from lower grade lesions, first defined by Scherer in the 1940s [2]. The rapid and de novo development of aggressive lesions is defined as primary GBM, accounting for approximately 95% of cases and thought to develop in part from a defined set of oncogenic mutations [6]. Secondary GBM cases have been identified as evolving from lower grade astrocytoma precursors, often distinguished by the presence of the isocitrate dehydrogenase 1 (IDH1) mutation and given a more favourable prognosis due to more frequent diagnosis in younger patients [6, 7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
