期刊
THERANOSTICS
卷 11, 期 5, 页码 2048-2057出版社
IVYSPRING INT PUBL
DOI: 10.7150/thno.53506
关键词
glioblastoma; fatty acids; metabolism; arginine; glutamine; autophagy
资金
- Mark Linder Walk for the Mind, Illinois Neurological Institute
- OSF foundation, Peoria, IL
- KB Strong Foundation, Washington, IL
- Illinois Neurological Institute Research Council
- William E. McElroy Charitable Foundation, Springfield, Illinois
Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults with a median survival of just 15 months; Researchers are focusing on targeting glucose metabolism to meet the increased demand for replication and progression in GBM; Despite the limited therapeutic interventions specifically targeting metabolic pathways in GBM, further insight is hoped to be gained through this review to develop novel treatment modalities.
Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. With a designation of WHO Grade IV, it is also the most lethal primary brain tumor with a median survival of just 15 months. This is often despite aggressive treatment that includes surgical resection, radiation therapy, and chemotherapy. Based on the poor outcomes and prevalence of the tumor, the demand for innovative therapies continues to represent a pressing issue for clinicians and researchers. In terms of therapies targeting metabolism, the prevalence of the Warburg effect has led to a focus on targeting glucose metabolism to halt tumor progression. While glucose is the dominant source of growth substrate in GBM, a number of unique metabolic pathways are exploited in GBM to meet the increased demand for replication and progression. In this review we aim to explore how metabolites from fatty acid oxidation, the urea cycle, the glutamate-glutamine cycle, and one-carbon metabolism are shunted toward energy producing pathways to meet the high energy demand in GBM. We will also explore how the process of autophagy provides a reservoir of nutrients to support viable tumor cells. By so doing, we aim to establish a foundation of implicated metabolic mechanisms supporting growth and tumorigenesis of GBM within the literature. With the sparse number of therapeutic interventions specifically targeting metabolic pathways in GBM, we hope that this review expands further insight into the development of novel treatment modalities.
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