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This Concept Map, created with IHMC CmapTools, has information related to: V08. Familial Adenomatous Polyposis -FAP, Migrates to nucleus and cuases Inappropriate gene expression, Appearance of polyps variously associated with Diets high in fat, Appearance of polyps variously associated with Gardners syndrome, Once 1 allele is knocked out, there is a high freq of somatic mutation this is Rate limiting step, Autosomal Dominant ie 50% chance of inheriting, Both alleles must be knocked out before adenomas form but is still considered dominant because Once 1 allele is knocked out, there is a high freq of somatic mutation, Regulator of Cell Adhesion, High risk of this happening in FAP patients due to Early development of Adenomas, 80% of sporadic cancers overall liftime 5 to 6 percent, Loss of function which allows Accumulation of Free Cytosolic B- Caratin, 50% chance of inheriting although 20-30% of cases are new germline mutatons, FAP accounts for less than 1% of colon cancer although 80% of sporadic cancers, Dysplastic groups implies Still need to acquire other mutations to proceed to cancer, Appearance of polyps variously associated with Hypertrophy of retinal pigment, 8. FAMILIAL ADENOMATOUS POLYPOSIS (FAP) inheritance non penetrance is rare, 2-3 per 100,000 but FAP accounts for less than 1% of colon cancer, 8. FAMILIAL ADENOMATOUS POLYPOSIS (FAP) etiology 15% of colorectal cancer is familial, APC gene normal function Regulator, Treatments aimed at stopping progression to cancer include Colectomy, 15% of colorectal cancer is familial including HNPCC)