Table 1.

Somatic mutation in WNT pathway genes in various cancers types*

Gene	Type of mutation	Primary tissues	Number of mutated samples	% mutated	Total samples
APC	Primarily frameshift and deletion mutations leading to compromised ability to degrade ATNNB1	Large intestine	2,152	39%	5,517
		Stomach	129	15%	214
		Soft tissue	50	12%	430
		Small intestine	34	16%	214
		Pancreas	26	14%	184
		Liver	11	12%	94
CTNNB1	Mutations in CTNNB1 cluster around the amino-terminus and prevent the phosphorylation amino acids, S33, S37, T41 and S45, resulting in impaired degradation of CTNNB1	Liver	907	23%	3,933
		Soft tissue	673	42%	1,601
		Endometrium	218	20%	1,098
		Kidney	168	14%	1,225
		Pancreas	125	26%	476
		Ovary	104	11%	913
		Adrenal gland	100	19%	534
		Pituitary	86	24%	360
		Biliary tract	43	10%	433
AXIN1	Many mutations prevent AXIN1 from acting as a scaffold to degrade CTNNB1	Biliary tract	10	38%	26
AXIN1		Liver	49	11%	448
WTX (also known as FAM123B)	Predicted to be loss-of-function mutations	Kidney	125	13%	949
WTX (also known as FAM123B)	Predicted to be loss-of-function mutations	Large intestine	19	13%	151
TCF7L2	Unknown	Large intestine	13	28%	47

*Cited from the Catalogue of Somatic Mutations in Cancer (COSMIC) database.