The Multifaceted Metabolism of Glioblastoma

  • Addison Quinones
  • Anne LeEmail author
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1063)


Glioblastoma multiforme (GBM) develops on glial cells and is the most common, as well as the deadliest, form of brain cancer [1]. As in pancreatic cancers, distinct combinations of genetic alterations in GBM subtypes induce a multiplicity of metabolic phenotypes, which explains the variability of GBM sensitivity to current therapies targeting its reprogrammed metabolism. Therefore, it is becoming imperative for cancer researchers to account for the metabolic heterogeneity within this cancer type before making generalized conclusions about a particular drug’s efficacy against all cancers of that type. GBMs can be classified initially into two subsets consisting of primary and secondary GBMs, and this categorization stems from cancer development. GBM is the highest grade of gliomas, which includes glioma I, glioma II, glioma III, and glioma IV (GBM). Secondary GBM develops from a low-grade glioma to advanced stage cancer, while primary GBM provides no signs of progression and is identified as an advanced stage glioma from the onset. The differences in prognosis and histology correlated with each classification are normally negligible, but the demographics of individuals affected and the accompanying genetic/metabolic properties show distinct differentiations [2].


Glioblastoma Metabolic profile Glutamine metabolism IDH1 mutation mTOR signaling Cysteine catabolism 







Bis-2-(5-Phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide


Cyclin-dependent kinase inhibitor 2A


Cysteine dioxygenase


Cysteine sulfinic acid


Epidermal growth factor receptor


Gamma-aminobutyric acid type A receptor alpha-1




Glutamate dehydrogenase








Isocitrate dehydrogenase


Macrophage 2


Myc-associated factor X


Mechanistic target of rapamycin or mammalian target of rapamycin


Neurofilament light


Neurofibromatosis type 1


Phosphoprotein 53


Platelet-derived growth factor receptor alpha


Pyruvate dehydrogenase


Phosphoinositide 3-kinase


Phosphatase and tensin homolog


Reactive oxygen species


Receptor tyrosine kinase


Solute carrier family 12 member 5


Synaptotagmin 1


Tricarboxylic acid


Ten-eleven translocation


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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of PathologyJohns Hopkins University School of MedicineBaltimoreUSA
  2. 2.Department of Pathology and OncologyJohns Hopkins University School of MedicineBaltimoreUSA

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