Role of abnormal lipid metabolism in development, progression, diagnosis and therapy of pancreatic cancer

Table 3 Oncogenes and tumor suppressor genes whose products alter the metabolism of pancreatic cancer cells

Gene	Protein	Mechanism of alteration in PDAC	Regulated processes in PDAC	Alteration in PDAC	Ref.
Oncogenes
KRAS	KRAS	Point mutations	Cell proliferation and survival, motility, glucose transport, glycolysis, hexosamine synthesis, nonoxidative pentose phosphate pathway arm, glutaminolysis	> 95%	[73,94,259-261]
AKT	AKT	Mutations, amplification	Signal transduction, lipogenesis, glucose transport	10%-20%	[73,79-81,262-264]
c-erbB2	HER2	Overexpression amplification	Proliferation, differentiation, survival	20%-80%	[265-268]
Myc	MYC	Amplification overexpression	Glycolysis, glutaminolysis, PDH inhibition	70%	[55,73,82,94,269]
Tumor suppressor genes
TP53	p53	Mutation and second allele deletion	Cell cycle, apoptosis, DNA repair, glucose transport, glycolysis, lipogenesis, ppp oxidative arm, glutaminolysis	50%-80%	[270-273]
Smad4/DPC4	SMAD4	Homozygous deletion, mutation and second allele deletion	Cell cycle, TGF-β signaling	55%	[274-276]
STK/LKB1	LKB1	Homozygous deletion, mutation and second allele deletion	Apoptosis, lipogenesis, energy production, protein synthesis	5%	[277-279]
CDKN2A/p16	p16	Homozygous deletion, mutation, hypermethylation	Cell cycle	95%	[280-282]
PTEN	PTEN	Hypermethylation, inhibition by miRNA	PI3K/AKT signaling pathway	30%-70%	[79,283,284]

PDAC: Pancreatic ductal adenocarcinoma.