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The Multifaceted Metabolism of Glioblastoma

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

Abstract

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].

Keywords

Glioblastoma Metabolic profile Glutamine metabolism IDH1 mutation mTOR signaling Cysteine catabolism 

Abbreviations

2HG

2-Hydroxyglutarate

aKG

Alpha-ketoglutarate

BPTES

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

CDKN2A

Cyclin-dependent kinase inhibitor 2A

CDO

Cysteine dioxygenase

CSA

Cysteine sulfinic acid

EGFR

Epidermal growth factor receptor

GABRA1

Gamma-aminobutyric acid type A receptor alpha-1

GBM

Glioblastoma

GDH

Glutamate dehydrogenase

GLS

Glutaminase

GSH

Glutathione

HK

Hexokinase

IDH

Isocitrate dehydrogenase

M2

Macrophage 2

MAX

Myc-associated factor X

mTOR

Mechanistic target of rapamycin or mammalian target of rapamycin

NEFL

Neurofilament light

NF1

Neurofibromatosis type 1

p53

Phosphoprotein 53

PDGFRA

Platelet-derived growth factor receptor alpha

PDH

Pyruvate dehydrogenase

PI3K

Phosphoinositide 3-kinase

PTEN

Phosphatase and tensin homolog

ROS

Reactive oxygen species

RTK

Receptor tyrosine kinase

SLC12A5

Solute carrier family 12 member 5

SYT1

Synaptotagmin 1

TCA

Tricarboxylic acid

TET

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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