Fig. 4
From: Metabolic gene alterations impact the clinical aggressiveness and drug responses of 32 human cancers
a Major catabolic and anabolic pathways of glucose and lipid metabolism in human cells. Nodes represent either enzymes (blue outline colour) or metabolic regulators (red outline colour). Node colours represent tumour suppressors (blue) and oncogenes (red) and their increasing colour intensities denote higher percentages of tumours with alterations in the genes encoding these enzymes or regulatory proteins. Edges indicate known types of interaction: red for inhibition and green arrows for activation. Abbreviations: GLUTs, all glucose transporters; HK, hexokinase; PFK, phosphofructokinase; PK, pyruvate kinase; LDH, lactate dehydrogenase; PDH, pyruvate dehydrogenase complex; PDK; pyruvate dehydrogenase kinase; CS, citrate synthase; ACO2, cis-aconitase; IDH, isocitrate dehydrogenase; OGDH, α-ketoglutarate; SDH, succinate dehydrogenase; SUCL, succinyl-CoA lyase; FH, fumarate hydratase; MDH, malate dehydrogenase; ACLY, ATP-dependent citrate lyase; ACC, acetyl-CoA carboxylase; FASN, fatty acid synthase; PTEN, phosphatase and tensin homologue; AMPK, 5’-AMP-activated protein kinase; mTORC1, mechanistic target of rapamycin complex-1; PI3K, phosphoinositide-3 kinase; SREBP, Sterol regulatory element-binding protein; Akt, RAC-alpha serine/threonine-protein kinase; Kras, Kirsten rat sarcoma viral oncogene homologue; Myc, MYC proto-oncogene; HIF1α, hypoxia-inducible factor 1-alpha; LKB1, Liver Kinase B1; p53, p53 tumour suppressor. b overall fraction of samples with the central metabolic pathways gene alterations across 32 human cancers
