Genes and the aetiology of colonic cancer.
Sansom O J et al 2007, Nature April 5th , vol 446, 676-679
The APC gene encodes the adenomatous polyposis coli tumour suppressor protein. Mutation of the germline characterizes familial adenomatous polyposis (FAP), an autosomal intestinal cancer syndrome. Inactivation of APC is also recognized as the key early event in the development of sporadic colorectal cancers1, and its loss results in constitutive activity of the β-catenin-Tcf4 transcription complex. The proto-oncogene c-MYC has been identified as a target of the Wnt pathway in colorectal cancer cells in vitro, in normal crypts in vivo’ and in intestinal epithelial cells acutely transformed on in vivo deletion of the APC gene; The role of Myc in the intestine after Ape loss has been studied , after deleting both Apc and Myc in the adult murine small intestine. Loss of Myc reversed the phenotypes of perturbed differentiation, migration, proliferation and apoptosis, which occur on deletion of Ape Myc is required for the majority of Wnt target gene activation following Apc loss. These data establish Myc as the critical mediator of the early stages of neoplasia following Ape loss.
This may appear obscure to Nutritionists.
If we are to break away from repeated mantras that certain food items are involved in the ain science will be seen as poking sticks down a rabbit hole and hoping for something to turn up.

blogger_blog:

www.nutrition-nutritionists.com

blogger_author:

Martin Eastwood

blogger_permalink:

/2007/04/genes-and-cancer-of-colon.html