Adenomatous polyposis coli gene

Minowa T et al. Proteomic analysis of the small intestine and colon epithelia of adenomatous polyposis coli gene-mutant mice by two-dimensional gel electrophoresis. Electrophoresis 2000 21 1782—1786. 

Miyaki M, Konishi M, Kikuchi-Yanoshita R, et al. Characteristics of somatic mutation of the adenomatous polyposis coli gene in colorectal tumors. Cancer Res 1994 54 3011-3020. 

The link between Cox-2 and polyps has been most extensively studied in an animal model of FAP, the adenomatous polyposis coli gene knockout mouse, which develops multiple intestinal polyps. In this model, both sulindac and a Cox-2 inhibitor are effective in producing regression of adenomas. When this knockout mouse was crossbred to a Cox-2 knockout mouse to produce a double adenomatous polyposis coli/Cox-2 knockout, the development of intestinal polyposis was markedly reduced (Oshima etal., 1996). 

Normally, cell proliferation and cell death are in a steady state, where the rate of proliferation is matched by the rate of apoptosis. Colon cancer, like other cancers, is caused by mutations in key components of regulatory pathways in this case mutations of the tumour-suppressor gene APC, the adenomatous polyposis coli gene. When APC is inactivated and turned off, the Wnt pathway, normally operative only in the embryo, is turned on. The Wnt pathway also plays a role in other cancers, for example in mammary tumours in mice and humans (for further information and literature references, see ref. 14). 

Groden J, Thliveris A, Samowitz W, Carlson M, Gelbert L, Albertsen H, et al. Identification and characterization of the familial adenomatous polyposis coli gene. Cell 1991 66 589-600. 

AJCC American Joint Committee on Cancer APC adenomatous polyposis coli (gene)... 

Nagase, H. and Nakamura, Y. (1993) Mutations of the APC (adenomatous polyposis coli) gene. Hum. Mutat.,... 

Groden, J Thliveris, A., Samowitz, W., Carlson, M., Gelbert, L., Albertsen, H., Joslyn, G., Stevens, J., Spirio, L. and Robertson, M. (1991) Identification and characterization of the Familial Adenomatous Polyposis Coli gene. Cell 66 589-600. 

Miyaki, M., Konishi, M., Kikuchi-Yanoshita, R., Enomoto, M., Igari, T., Tanaka, K., Muraoka, M., Takahashi, H., Amada, Y., Fukayama, M., Maeda, Y., Iwama, T., Mishima, Y., Mori, T, and Koike, M. (1994) Characteristics of somatic mutation of the adenomatous polyposis coli gene in colorectal tumors. Cancer Res., 54 (11), 3011-3020. 

Adenomatous polyposis coli (APC) gene A tumor suppressor gene, acting as a gatekeeper to prevent development of tumors. A familial cancer syndrome called FAP, or familial adenomatous polyposis, is caused by mutations in APC. Mutation of APC also occurs commonly in sporadic cases of colorectal carcinoma. 

Since this promoter can be induced by the addition of zinc, it allows for the conditional expression of genes. This induction is especially important if the expression of a particular gene is deleterious to the cell. For example, the adenomatous polyposis coli (APC) tumor suppressor gene was inserted into a vector downstream of the MT II promoter (Morin et al., 1996). Since continuous expression of APC is inhibitory to cell growth, an inducible expression system was necessary to examine the effects of APC expression on cells. This promoter was specifically chosen due to its low basal activity in the absence of zinc The drawbacks to this system are the potential effects that increased zinc concentrations may have in the cell. These effects may include toxicity to the cell or altered gene expression due simply to the presence of zinc. 

The adenomatous polyposis coli tumour suppressor gene... 

APC, antigen-presenting cells are bone-marrow-derived cells, macrophages and dendritic cells which process foreign antigens and present them to T cells, OR, adenomatous polyposis coli protein, enoded by the human ape gene. 

The most common genetic alteration identified to date is LOH of the highly imprinted region of chromosome lip near the WT2 gene locus.Additionally, alterations in the adenomatous polyposis coli (APC)/ -catenin pathway have been reported in 50% to 80% of pancreatoblastomas.Most often, these involve the p-catenin gene (CTNNBlj. ssooo u Uke DAs, TP53 and KRAS mutations have not been detected.334.299,30i,302... 

We applied SOMA to genotyping several variant sites in the human adenomatous polyposis coli (APC) gene. The first of these is a variant (I1307K) present in 6% of the Ashkenazi Jewish population that is associated with an inaeased risk of colorectal cancer of approximately two fold [22]. The polymorphism is an A to T change at codon 1307 and hence represents the most difficult alteration to analyse because there is only a 9Da mass difference between the two variants. PCR primers were designed to yield 15-mer oligonucleotides for MS analysis following... 

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