Mutational inactivation of the β- catenin destruction complex
此为经典模式，即 archetypal mode
APC、AXIN1和AXIN2的失活突变或激活β-连环蛋白(由CTNNB1编码)本身
Misregulation of WNT receptor abundance
WNT受体丰度失调
loss of RNF43 and NRF3
RNF43和ZNRF3缺乏的细胞已不再需要RSPO，表现出肿瘤细胞特征：小环境独立生长
acquired RSPO overexpression
细胞表面过多表达WNT受体，促进WNT依赖肿瘤的生长
Tissue specificity
组织特异性
各种肿瘤WNT信号通路突变呈现特异性
比如：In colorectal cancer (CRC; n = 594), the largest fraction
of sporadic tumours accumulates APC mutations (67%),
followed by lower fractions of RNF43 (8%), CTNNB1
(6%) and AXIN2 (5%) mutations.
WNT通路对癌症的贡献可能比TCGA中表现的还要大
由于检测方法的问题
WNT path way regulators may be downregulated by promoter hypermethylation
WNT通路可能被启动子超甲基化下调
Tumour subtypes and prognosis
肿瘤的亚型和预后
different WNT pathway mutations are not equal
结直肠癌
过往研究
APC突变会导致家族性腺瘤性息肉病(Fap)
APC mutations are an early and perhaps rate- limiting event
