A s of 1999, it is possible to test selected subjects for carriage of germline mutations in genes responsible for familial adenomatous polyposis (FAP), 1,2 hereditary nonpolyposis colorectal cancer (HNPCC), 3,4 Peutz-Jeghers syndrome, 5 and juvenile polyposis. 6,7 These diseases are heterogeneous ph
Familial adenomatous polyposis : Discovery of a family and its management in a cancer genetics clinic
β Scribed by Henry T. Lynch; Susan T. Tinley; Jane Lynch; Jon Vanderhoof; Stephen J. Lemon
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 158 KB
- Volume
- 80
- Category
- Article
- ISSN
- 0008-543X
No coin nor oath required. For personal study only.
β¦ Synopsis
hereditary cancer. The adenomatous polyposis coli (APC) germline mutation, when identified within an
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Hereditary cancer represents approximately 5-10% of the total cancer burden and may account for 60,000 to 120,000 new cancer occurrences this year in the United States. New developments in molecular genetics and the cloning of cancer-prone genes have intensely fueled interest in dealing with heredit
A family is presented with attenuated familial adenomatous polyposis of variable phenotype. The clinical features range from sparse right-sided polyposis and cancer in the proximal colon at the age of 34 to pan-colonic polyposis and cancer at the age of 68. Rectal sparing is common to all affected m