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)|
|Number of pages||10|
|Journal||Advances in experimental medicine and biology|
|State||Published - Dec 1 2000|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)