Table 2.

Recurrent somatic genetic alteration in gastric cancer analyzed using next-generation sequencing

Gene	Classification	Core pathway	Process	Mutational rate (%)			Reference
				Previous study	Hypermutated tumora	Nonhypermutated tumora
TP53	TSG	Cell cycle/apoptosis, DNA damage control	Cell survival	14–59	35	50	27,116–118,123–127
PIK3CAb	Oncogene	PI3K-AKT	Cell survival	7–36	40	12	27,116–118,123–127
CDH1c	TSG	APC	Cell fate	4–36	-	11	27,116–118,124–126
ARID1Ab	TSG	Chromatin modification	Cell fate	8–27	44	14	27,116,118,123–126
PTEN	TSG	PI3K-AKT	Cell survival	0–27	13	-	27,116,123,125,127
KRAS	Oncogene	RAS/RAF	Cell survival	0–27	19	6	27,116,118,125,127
RHOAc	Oncogene	RHO/ROCK	Cell survival	0–23	-	6	27,116,118
APC	TSG	APC	Cell fate	3–14	-	7	27,116,118,123,124
ERBB3	Oncogene	RTK	Cell survival	0–10	25	-	27,116
ERBB2	Oncogene	RTK	Cell survival	2–9	-	3	27,116,118,126,127
CTNNB1	Oncogene	APC	Cell fate	2–9	-	4	27,116,118,124
MET	Oncogene	RTK	Cell survival	0–9		-	116,127
FBXW7	TSG	NOTCH	Cell fate	2–6	24	-	27,118,127
SMAD4	TSG	TGF-β	Cell survival	4–6	-	8	27,118
EGFR	Oncogene	RTK	Cell survival	0–6	-	-	27,116,127
NRAS	Oncogene	RAS/RAF	Cell survival	0–5	-	-	116,125,127

TSG, tumour suppressor gene; PI3K, phosphoinositide 3-kinase; RTK, receptor tyrosine kinase; TGF-β, transforming growth factor β.

^aData of mutation rates are from The Cancer Genome Atlas database; [25]

^bMore frequently mutated gene in gastric cancer with microsatellite instability–high frequency feature or Epstein-Barr virus positivity;

^cMore frequently mutated gene in gastric cancer with diffuse type of Lauren classification.