APC, Signal transduction and genetic instability in colorectal cancer

By R. Fodde, R. Smits, Hans Clevers. Nature Reviews. Cancer, 2001

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E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, neutral): “[51] 154 Cancer Metastasis Rev (2009) 28:151–166”
On the road to cancer: aneuploidy and the mitotic checkpoint (2005, background): “Truncated forms of APC can kill two birds with one stone — not only are they responsible for increased cell proliferation, owing to a failure to degrade β-cateni”
Canonical Wnt signals are essential for homeostasis of the intestinal epithelium. (2003, background): “Second, mutations that activate the Wnt/ -catenin pathway can lead to colorectal cancer in humans (Powell et al. 1992; Kinzler and Vogelstein 1996; Fodde et al. 2001) as well as adenomatous polyp formation in the mouse intestine (Moser et al. 1990; Fodde et al. 1994; Oshima et al. 1995; Shibata et…”
Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer (2004, background): “jpg" NDATA ITEM> ]> Aberrant WNT pathway signaling is an early progression event in 90% of colorectal cancer”
The ins and outs of APC and β‐catenin nuclear transport (2002, background): “Nuclear accumulation of β-catenin is also observed in cancers resulting from mutations in the β-catenin, adenomatous polyposis coli (APC) or Axin genes (Polakis, 2000; Fodde et al., 2001).”
Interplay of cadherin-mediated cell adhesion and canonical Wnt signaling. (2010, neutral): “– Wnt signaling (Kinzler and Vogelstein 1996; Huelsken et al. 2000; Fodde et al. 2001).”