The adenomatous polyposis coli protein (APC) is mutated in familial adenomatous polyposis patients as well as in sporadic colorectal tumors. In an attempt to further understand the function of APC, the subcellular localization of APC was examined. Wild-type and mutant forms of APC were expressed in mammalian cells and protein detected by immunofluorescence using monoclonal and polyclonal antibo...

Colorectal cancer is undoubtedly one of the most genetically studied malignancies. In the past 20 years, substantial progress has been made in understanding the genetic and molecular pathogenesis of this cancer. It is instructive that the genes involved in the inherited colon cancer syndromes are the same genes involved in the etiology of most colorectal cancers. Familial adenomatous polyposis ...

Analysis of two human familial cancer syndromes, hereditary nonpolyposis colorectal cancer and familial adenomatous polyposis, indicates that mutations in either one of four DNA mismatch repair gene homologues or the adenomatous polyposis coli (APC) gene, respectively, are important for the development of colorectal cancer. To further investigate the role of DNA mismatch repair in intestinal tu...

The APC (adenomatous polyposis coli) gene is responsible for familial adenomatous polyposis and is also associated with the development of sporadic tumors of the colon and stomach. To investigate whether or not mutations of APC play any role in tumors arising in other organs, we examined somatic mutations of this gene in sporadic (nonfamilial) renal cell carcinomas, hepatocellular carcinomas, a...

Testing for adenomatous polyposis coli (APC), the gene responsible for familial adenomatous polyposis (FAP), can now be offered to family members in FAP kindreds. With the availability of this test, genetic counseling has become a crucial tool for helping FAP patients and their relatives understand the syndrome and its implications and for assisting at-risk individuals in making informed decisi...

We describe 2 extended kindreds supposedly manifesting familial multiple adenomatous polyposis coli (FPC), but which show marked heterogeneity in the phenotypic expression of colorectal adenomatous polyps. In one family, 2 individuals had diffuse polyposis at very early ages (7 and 10 years), while 6 others (aged 23 to 72 years) had solitary polyps only. Of the patients with solitary polyps, 2 ...

Analysis of two human familial cancer syndromes, hereditary nonpol yposis colorectal cancer and familial adenomatous polyposis, indicates that mutations in either one of four DNA mismatch repair gene homo logues or the adenomatous polyposis coli (APC) gene, respectively, are important for the development of colorectal cancer. To further investigate the role of DNA mismatch repair in intestinal ...

Diverse cellular proteins and RNAs are tightly regulated in their subcellular localization to exert their local function. Here we report that the tumour suppressor adenomatous polyposis coli protein (APC) directs the localization and assembly of human immunodeficiency virus (HIV)-1 Gag polyprotein at distinct membrane components to enable the efficient production and spread of infectious viral ...

Familial adenomatous polyposis (FAP) is responsible for <1% of colorectal cancer (CRC) cases and is inherited an autosomal dominant trait. Patients generally present hundreds to thousands of adenomas and develop colorectal cancer by age 35- 40 if left untreated. Here we report four patients with germline frameshift mutation (small deletion) at exon 15 of adenomatous polyposis coli (APC) tumor s...

Familial adenomatous polyposis, an autosomal-dominantly inherited colorectal cancer predisposition syndrome, is caused by germ-line mutations in the adenomatous polyposis coli (APC) gene. Despite the use of different screening methods, studies worldwide fail to identify APC mutations in 20-50% of all familial adenomatous polyposis patients (APC mutation-negatives). In this study, missense mutat...