Laura M. Shelton

TL;DR: Evidence is reviewed supporting a general hypothesis that genomic instability and essentially all hallmarks of cancer, including aerobic glycolysis (Warburg effect), can be linked to impaired mitochondrial function and energy metabolism.

TL;DR: A key role is identified for serine and glycine metabolism in the survival of brain cancer cells within the ischaemic zones of gliomas and SHMT2 activity limits that of pyruvate kinase and reduces oxygen consumption, eliciting a metabolic state that confers a profound survival advantage to cells in poorly vascularized tumour regions.

TL;DR: A competitive and partially redundant relationship between transaminases and GLUD is described, and they reveal how coupling of glutamate-derived carbon and nitrogen metabolism can be regulated to support cell proliferation.

TL;DR: A metabolic adaptation that is required for hypoxia-induced BCSC enrichment and metastasis is reported, highlighting a role for PHGDH in the formation of secondary cancers and potential implications for therapeutic targeting of advanced cancers.

TL;DR: This work proposes an alternative approach to brain cancer management that exploits the metabolic flexibility of normal cells at the expense of the genetically defective and metabolically challenged tumor cells.