Abstract
The adenomatous polyposis coli (APC) gene has been found to be mutated during the development of sporadic colorectal tumours as well as in familial adenomatous polyposis patients (FAP), mutations being somatic or germinal respectively. The gene product is truncated in the carboxyterminal region but the role of the APC protein in tumorigenesis is not well understood. The purpose of this review is to reassess studies on the APC protein in an attempt to understand how the loss of its functions may cause or contribute to the development of carcinomas.
MeSH terms
-
Adenomatous Polyposis Coli / genetics*
-
Adenomatous Polyposis Coli Protein
-
Apoptosis
-
Cell Cycle
-
Colorectal Neoplasms / genetics*
-
Colorectal Neoplasms / physiopathology
-
Cytoskeletal Proteins / genetics*
-
Cytoskeletal Proteins / metabolism
-
Cytoskeletal Proteins / physiology
-
Gene Expression Regulation, Neoplastic
-
Humans
-
Microtubule-Associated Proteins / metabolism
-
Proteins / metabolism
-
Trans-Activators*
-
beta Catenin
Substances
-
Adenomatous Polyposis Coli Protein
-
CTNNB1 protein, human
-
Cytoskeletal Proteins
-
Microtubule-Associated Proteins
-
Proteins
-
Trans-Activators
-
beta Catenin