Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene occurs in most colorectal cancers. The proto-oncogene c-MYC was one of the first genes linked to APC inactivation, but the in vivo significance of c-MYC's enhanced expression in intestinal cells with APC defects has been uncertain. Sansom et al. recently reported that targeted inactivation of c-Myc in murine intestinal epithelium potently inhibited phenotypical and transcriptional changes seen in Apc-deficient intestinal epithelium. While these findings are very interesting, some questions remain about the assignment of c-Myc as the pre-eminent β-catenin-regulated gene in intestinal epithelium
The capacity to model cancer within the mouse has advanced significantly in recent years. Perhaps th...
The APC gene is mutated both in familial adenomatous polyposis (FAP) and sporadic colorectal cancers...
Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene strongly predispose to devel...
Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene occurs in most colorectal...
The Adenomatous polyposis coli (Apc) gene is mutated in up to 80% of sporadic colorectal cancers. Af...
The APC gene encodes the adenomatous polyposis coli tumour suppressor protein, germline mutation of...
Within the intestinal epithelium, c-Myc has been characterized as a target of β-catenin-TCF signalli...
The Myc transcription factor is a potent inducer of proliferation and is required for Wnt/-catenin s...
Abstract Inactivation of the gene encoding the adenomatous polyposis coli (APC) tumour suppressor pr...
The use of mouse models to study neoplasia is proving particularly powerful in dissecting the mechan...
Mutation of the tumor suppressor adenomatous polyposis coli (APC) is considered an initiating step i...
Aberrant Wnt signaling mediated by mutations affecting APC (adenomatous polyposis coli) or β-catenin...
Adenomatous polyposis coli (APC) mutations are found in most colorectal tumours. These mutations are...
Loss of the APC (adenomatous polyposis coli) gene in colorectal cancer leads to a rapid deregulation...
AbstractThe adenomatous polyposis coli (APC) tumor suppressor protein is inactivated by mutations in...
The capacity to model cancer within the mouse has advanced significantly in recent years. Perhaps th...
The APC gene is mutated both in familial adenomatous polyposis (FAP) and sporadic colorectal cancers...
Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene strongly predispose to devel...
Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene occurs in most colorectal...
The Adenomatous polyposis coli (Apc) gene is mutated in up to 80% of sporadic colorectal cancers. Af...
The APC gene encodes the adenomatous polyposis coli tumour suppressor protein, germline mutation of...
Within the intestinal epithelium, c-Myc has been characterized as a target of β-catenin-TCF signalli...
The Myc transcription factor is a potent inducer of proliferation and is required for Wnt/-catenin s...
Abstract Inactivation of the gene encoding the adenomatous polyposis coli (APC) tumour suppressor pr...
The use of mouse models to study neoplasia is proving particularly powerful in dissecting the mechan...
Mutation of the tumor suppressor adenomatous polyposis coli (APC) is considered an initiating step i...
Aberrant Wnt signaling mediated by mutations affecting APC (adenomatous polyposis coli) or β-catenin...
Adenomatous polyposis coli (APC) mutations are found in most colorectal tumours. These mutations are...
Loss of the APC (adenomatous polyposis coli) gene in colorectal cancer leads to a rapid deregulation...
AbstractThe adenomatous polyposis coli (APC) tumor suppressor protein is inactivated by mutations in...
The capacity to model cancer within the mouse has advanced significantly in recent years. Perhaps th...
The APC gene is mutated both in familial adenomatous polyposis (FAP) and sporadic colorectal cancers...
Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene strongly predispose to devel...