Table 3.

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

Gene	Classification	Core pathway	Process	Mutational rate (%)			Reference
				Previous study	Hypermutated tumora	Nonhypermutated tumora
TP53b	TSG	Cell cycle/apoptosis, DNA damage control	Cell survival	27–65	20	60	119–121,128,129
KRASb	Oncogene	RAS/RAF	Cell survival	33–58	30	43	119–121,128–131
APCb,c	TSG	APC	Cell fate	40–56	51	81	121,129
PIK3CAb	Oncogene	PI3K-AKT	Cell survival	14–20	-	18	119,120,128,129,131
BRAFc	Oncogene	RAS/RAF	Cell survival	5–14	46	-	119,120,128–131
PTEN	TSG	PI3K-AKT	Cell survival	2–13	-	-	119,128,129
EGFR	Oncogene	RTK	Cell survival	0–11	-	-	128,129,131
SMAD4b	TSG	TGF-β	Cell survival	2–11	-	10	119,121,128,129
FBXW7b	TSG	NOTCH	Cell fate	4–10	-	11	119,120,128,129
NRAS	Oncogene	RAS	Cell survival	2–7	-	9	119,120,128–131
MET	Oncogene	RTK	Cell survival	2–4	-	-	119,120
CTNNB1	Oncogene	APC	Cell fate	1–4	-	5	121,128,129
AKT1	Oncogene	PI3K	Cell survival	1–4	-	-	119,128,129
ERBB2	Oncogene	RTK	Cell survival	1–3	-	-	128,129
ALK	Oncogene	RTK	Cell survival	1–2	-	-	120,128,129
MAP2K1	Oncogene	RAS/RAF	Cell survival	0–2	-	-	119–121,128

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; [26]

^bMore frequently mutated gene in nonhypermutated colorectal cancer;

^cMore frequently mutated gene in hypermutated colorectal cancer.