Ontology highlight
ABSTRACT:
SUBMITTER: Amos-Landgraf JM
PROVIDER: S-EPMC3277532 | biostudies-literature | 2012 Feb
REPOSITORIES: biostudies-literature
Amos-Landgraf James M JM Irving Amy A AA Hartman Cory C Hunter Anthony A Laube Brianna B Chen Xiaodi X Clipson Linda L Newton Michael A MA Dove William F WF
Proceedings of the National Academy of Sciences of the United States of America 20120123 6
Studies of tumors from human familial adenomatous polyposis, sporadic colon cancer, and mouse and rat models of intestinal cancer indicate that the majority of early adenomas develop through loss of normal function of the Adenomatous polyposis coli (APC) gene. In murine models of familial adenomatous polyposis, specifically the multiple intestinal neoplasia mouse (Min) and the polyposis in the rat colon (Pirc) rat, most adenomas have lost their WT copy of the Apc gene through loss of heterozygos ...[more]