TABLE 1

Common genetic alterations of Wnt pathway components in human cancers

Gene	Type of Mutation	Primary Tissues	% Mutated	Reference
APC	Mainly frameshift and nonsense mutations that lead to truncated APC proteins with compromised ability to degrade β-catenin; LOH	Large intestine	70	^a
		Stomach	13	^a
		Endometrium	7	^a
		Liver	2.7	^a
AXIN1	Mainly missense mutations, truncating mutations, and deep deletions	Liver	7	^a
		Stomach	3	^a
		Large intestine	2.5	^a
CTNNB1	Mainly missense mutations in the N-terminal Ser/Thr phosphorylation sites of β-catenin that prevent its degradation	Liver	29	^a
		Endometrium	18	^a
		Adrenal cortex	16	^a
		Large intestine	6	^a
		Stomach	6	^a
		Pancreas	2.7	^a
RNF43	Mainly missense mutations and truncating mutations due to frameshift or nonsense mutations, LOH, and homozygous deletion	Ovary (mucinous carcinoma/mucinous borderline tumor)	21/9	Ryland et al., 2013
		Stomach	13	^a
		Biliary tract (liver fluke-associated cholangiocarcinoma)	9.3	Ong et al., 2012
		Large intestine	9	^a
		Pancreas	7	^a
		Endometrium	4	^a
ZNRF3	Mainly missense mutations and truncating mutations due to frameshift or nonsense mutations, LOH, and homozygous deletion	Adrenal cortex	20	^a
		Large intestine	4	^a
		Stomach	2.1	^a
RSPO2	Chromosome rearrangement leading to the recurrent EIF3E-RSPO2 gene fusions	Large intestine	2.9	Seshagiri et al., 2012
RSPO2		Others (lung, head and neck, esophagus, stomach, ovary, and breast)	1–2	Cardona et al., 2014; Li et al., 2018
RSPO3	Chromosome rearrangement leading to the recurrent PTPRK-RSPO3 gene fusions	Large intestine	7.4	Seshagiri et al., 2012
RSPO3		Others (lung, head and neck, esophagus, ovary, and breast)	1–11	Cardona et al., 2014

LOH, loss of heterozygosity.
↵^a Curated from the cBioPortal database (https://www.cbioportal.org) in July 2019.