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. 2017 Jan 8;9(1):1–17. doi: 10.4254/wjh.v9.i1.1

Table 1.

Significantly altered metabolites in hepatocellular carcinoma patients vs cirrhosis controls

Ref. Platform Tissue (organism) HCC etiology Significantly altered metabolites in HCC patients vs cirrhosis controls Main pathways distinguishing HCC from cirrhosis
Patterson et al[29] UPLC/QTOF-MS; UPLC/ESI-TQMS; GC/MS Plasma (human) HCC n = 20: LPC (14:0) ↓ LPC metabolism
EtOH n = 6 LPC (18:1) ↓
HBV n = 3 LPC (20:4) ↓
HCV n = 5 LPC (20:3) ↓
NASH n = 3 LPC (22:6) ↓
NASH/alcoholic steatohepatitis n = 1 FFA (24:0) - lignoceric acid ↓ Very long chain fatty acid metabolism
HH n = 2 FFA (24:1) - nervonic acid ↓ Hemoglobin metabolism
Bilirubin ↑
Biliverdin ↑
Xiao et al[37] UPLC/QTOF-MS Serum (human) HCV 3β, 6β-dihydroxy-5β-cholan-24-oic acid ↓ Bile acid biosynthesis
3α, 7β-dihydroxy-5β-cholest-24-en-26-oic acid ↓
GCA ↓
GDCA ↓
GCDCA ↓
TCDCA ↓
Linoelaidyl carnitine ↓ CPT shuttle system
Oleoylcarnitine ↓
Palmitoyl carnitine ↓
O-octanoyl-R-carnitine ↓
LPC (20:1) ↓ LPC metabolism
LPC (20:4) ↓
PE (20:4/18:1) ↓
4E;15Z-Bilirubin IXa ↓ Hemoglobin metabolism
15,16-dihydrobiliverdin ↓
3-ganidinopropionicacid ↓
Tetracosahexaenoic acid ↓ Eicosanoid metabolism
3-hydroxy-eicosanoic acid ↓
Oleamide ↓
Phe-Phe ↑
Wang et al[38] UPLC/MS-MS; LC/QTOF-MS Serum (human) HCC n = 82: LPC-16:0 ↑ LPC metabolism
HBV-cirrhosis n = 41 LPC-18:0 ↑
HBV-only n = 41 16:0/18:1-PC ↑
16:0/18:2-PC ↑
16:0/20:4-PC ↑
16:0/22:6-PC ↑
18:0/18:2-PC ↑
Phenylalanine ↓ Gut flora metabolism
GCDCA ↓ Bile acid metabolism
Canavaninosuccinate ↑↑ Organic acid metabolism
Zhou et al[39] UPLC/QTOF-MS Serum (human) HCC n = 69: LPC (14:0) HCC-C ↓ LPC metabolism
HBV-HCC (HCC-B) n = 38 LPC (16:1) HCC-C ↓
HCV-HCC (HCC-C) n = 31 LPC (18:3) HCC-B ↓
HCC-C ↓
LPC (18:2) HCC-B ↓
HCC-C ↓
LPC (18:1) HCC-B ↓
HCC-C ↓
LPC (18:0) HCC-C ↓
LPC (20:5) HCC-C ↓
LPC (20:4) HCC-B ↓
HCC-C ↓
LPC (20:3) HCC-B ↓
HCC-C ↓
LPC (20:2) HCC-C ↓
LPC (20:0) HCC-B ↓
HCC-C ↓
LPC (22:6) HCC-C ↓
LPC (22:5) HCC-B ↓
HCC-C ↓
LPC (22:4) HCC-B ↓
HCC-C ↓
Wu et al[31] SELDI-TOF-MS; HPLC/MS Serum (human) HBV GRO-α ↑ Cytokine
Thrombin light chain ↑ Protease cleavage
Ressom et al[36] UPLC/QTOF-MS Serum (human) HCC n = 78: GDCA ↓ Bile acid metabolism
→ HCV 67% TCA ↓
→ HBV 15% TCDCA ↓
→ Alcoholism 29% Sphingosine 1-phosphate ↑ Sphingolipid metabolism
→ NASH 13% LPC (16:0) ↑ LPC metabolism
→ Cryptogenic (8%) LPC (17:0) ↑
→ Autoimmune (3%) LPC (18:0) ↑
LPC (15:0) ↑
LPC (22:6) ↑
LPE (22:6) ↑
LPE (20:4) ↑
LPE (20:3) ↑
PS ↑
Yang et al[28] HRMAS 1H NMR Biopsy (human) HCC n = 17: Glucose ↓ Glycolysis
→ Cirrhosis n = 9 Creatine ↓
→ No cirrhosis n = 8 PE ↑ LPC metabolism
Glutamine ↑ Amino acid metabolism
Glutamate ↑
PC + GPC ↑ Bile acid metabolism
Nahon et al[40] NMR Serum (human) EtOH cirrhosis High density lipoproteins HDL biosynthesis
Acetate ↑ Ketone body metabolism
N-acetyl-glycoproteins ↑ N-acetylglycoprotein
Glutamate ↑ Amino acid metabolism
Glutamine ↓
Budhu et al[43] GC/MS, UPLC/MS-MS Biopsy samples (human) HCC n = 356 Study reported on markers involved in cancer aggressivity through comparison of stem-like HCC to less benign mature hepatocyte HCC N/A
Training cohort n = 30
Testing cohort n = 217
Validation cohort n = 139
Beyoğlu et al[44] GC/MS Biopsy samples (human) Six HCC subtypes, liver fibrosis status unknown Glucose ↓ Glycolysis
Glycerol 3-phosphate ↓
Glycerol 2-phosphate ↓
Malate ↓
Alanine ↓
Myo-inositol ↓ PI3K pathway
Linoleic acid ↓ Prostaglandin biosynthesis
Fitian et al[45] UPLC/MS-MS and GC/MS Serum (human) HCV cirrhosis-associated HCC n = 30 Sphingosine ↑ Sphingolipid
HCV-cirrhosis n = 27 Xanthine ↑ Oxidative stress metabolism
Healthy volunteers n = 30 2-Pyrrolidinone ↑ GABA metabolism
2-Hydroxybutyrate ↑ Oxidative stress metabolism
Serine ↑ Amino acid
Glycine ↑
Aspartate ↑
12-HETE ↑ Inflammation pathway
15-HETE ↑
Isovalerate ↑ Gut microflora metabolism
Dihomo-linolenate ↑ Inflammation pathway
Gao et al[46] GC-TOF/MS Serum (human) HBV cirrhosis-associated HCC n = 39 Stearic acid Fatty acid biosynthesis
HBV-cirrhosis (n = 52) Heptadecanoic acid
Palmitic acid
5-Aminovaleric acid Gut microflora metabolism
Cholesterol ↑ Cholesterol metabolism
3-hydroxybutyric acid ↑ Ketogenesis
Malic acid ↑ TCA metabolism
Glutamine ↑ Amino acid
Asparagine ↓
Alanine ↑
Threonine ↓
Leucine ↓
Glutamic acid ↑
β-glutamate ↑
5-oxoproline ↓ Glutathione metabolism
1,2,4-cyclopropranodicarboxylic acid ↓ Dicarboxylic acid metabolism

Pathways of importance in the comparison of (1A) HCC vs cirrhosis and (2) cirrhosis vs healthy controls are shown. Arrows indicate the metabolite’s expression in cases vs appropriate controls. P < 0.05 was used as the significance level and metabolites reported in table are those which were most significantly upregulated or downregulated in each study. EtOH: Alcohol; TOCSY: Total correlation spectroscopy; HH: Hereditary hemochromatosis; TCA: Tricarboxylic acid; UPLC: Ultrahigh-performance liquid chromatography; QTOF: Quadrupole time of flight; SELDI: Surface-enhanced laser desorption/ionization; HRMAS: High-resolution magic angle spinning; LPE: Lysophosphatidyethanolamine; LPC: Lysophosphatidylcholine; HCC: Hepatocellular carcinoma; MS: Mass spectrometry; TOF: Time-of-flight; GC: Gas chromatography; LC: Liquid chromatography; NMR: Nuclear magnetic resonance; HBV: Hepatitis B virus; HCV: Hepatitis C virus; NASH: Non-alcoholic steatohepatitis; FFA: Free fatty acids; PE: Phosphorylethanolamine; GABA: γ-aminobutyric acid.