Carcinogenesis in familial polyposis coli

The inherited cancer disease familial polyposis coli (FPC) provides an excellent model not only for studying tumor progression in colorectal cancer but also for elucidating molecular mechanism of carcinogenesis in general. This paper reviews recent remarkable progress in the molecular mechanism of tumorigenesis in FPC. Included in this review is information on the localization of the FPC major gene and several types of genetic alterations during the development of tumors. One of these genetic alterations is activation of oncogenes such as mutated ras genes and another is inactivation of tumor suppression genes such as loss of heterozygosity. The mutated FPC gene on chromosome 5 q would be expected to be an early event to initiate the requisite hyperproliferation for adenoma formation. Adenomas will have undergone several gene or chromosome mutations before reaching the fully malignant state.