Table 1.
CRC | HCC | PDAC | REFERENCES | |
---|---|---|---|---|
% of human tumors containing mutations in key members of Wnt/β-catenin pathway | 90% of CRC | 18–44% of HCC | Rare in PDAC | reviewed in 17,18 52–54, 56–58 100,102,103 |
% of human tumors with β-catenin staining | 58–80% nuclear 100% membrane and cytoplasmic |
17–43% nuclear 57–62% membrane and cytoplasmic |
4–11% nuclear 35–65% cytoplasmic |
20–22 91–94 102,113,118–121 |
Wnt/β-catenin pathway members mutated most often | 80% APC 10% β-catenin |
3–44% β-catenin 5–25% AXIN1 Not APC |
Not seen in PDAC | reviewed in 18 52–54,56–58 100,102,103 |
Effects of Wnt/β-catenin hyperactivation in murine tumor models | Initiating event in tumorigenesis and is sufficient for tumor formation (adenomas not carcinomas) | Not sufficient for malignant transformation, but promotes tumorigenesis | Antagonizes Kras-initiated mPanIN and PDAC | reviewed in 17,18 70–72 107,109,110 |
Necessity of temporal regulation of Wnt/β-catenin pathway in tumorigenesis | No | No | Yes | reviewed in 17,18 70–72 107,109,110 |
Crosstalk with other signaling pathways (not an exhaustive list) | Notch, Hedgehog | TGF-β, HGF/MET | TGF-β, Hedgehog, Notch |
48–50 60,86,88 113–115 |