Abstract
The molecular events that contribute to the progression of colon cancer are beginning to unravel. An initiating and probably obligatory event is the oncogenic activation of β-catenin. This can come about by the loss of its negative regulator the adenomatous polyposis coli (APC) protein, or by mutations in the β-catenin gene that result in a more stable protein product. The interaction between APC and β-catenin, and additional proteins that affect assembly and signaling along this pathway, are discussed.
Original language | English (US) |
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Pages (from-to) | 23-32 |
Number of pages | 10 |
Journal | Advances in experimental medicine and biology |
Volume | 470 |
State | Published - Dec 1 2000 |
Externally published | Yes |
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)