The Multifaceted Metabolism of Glioblastoma

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].