Registration enables users to use special features of this website, such as past
order histories, retained contact details for faster checkout, review submissions, and special promotions.
Registration enables users to use special features of this website, such as past
order histories, retained contact details for faster checkout, review submissions, and special promotions.
Registration enables users to use special features of this website, such as past
order histories, retained contact details for faster checkout, review submissions, and special promotions.
Registration enables users to use special features of this website, such as past
order histories, retained contact details for faster checkout, review submissions, and special promotions.
Adenomatous polyposis coli (APC) is a gene frequently mutated in colorectal cancer and inherited mutations in this gene are causative for classical familial adenomatous polyposis. This gene is involved in the regulation of cell adhesion through its interaction with CDH1 (e-cadherin) and CTNNB1 (beta-catenin) via the WNT signaling pathway, and it is considered a tumor suppressor. The loss of functional APC protein (often alongside mutations in TP53 or KRAS) is a frequent event in colorectal cancers and is associated with cellular over-proliferation, chromosomal instability and carcinogenesis. In immunohistochemistry of normal tissue, APC has membranous and cytoplasmic positivity in most tissues throughout the body.
References: N Engl J Med. 2009 Dec 17;361(25):2449-60, PMID: 20018966; Gastroenterology. 2010 Jun;138(6):2059-72, PMID: 20420946;