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Deregulation of beta-catenin activity is an important step in the development of colorectal cancers. One consequence of this is transcriptional activation of cyclin D1, an oncogene known to be overexpressed in colorectal cancers. We tested the hypothesis that cyclin D1 gene activation is important for intestinal tumorigenesis. Multiple intestinal neoplasia mice (a model for human familial adenomatous polyposis) were crossed with cyclin D1 knockout (Ccnd1(-/-)) mice. Despite the absence of cyclin D1, intestinal tumors still developed. However, Ccnd1(-/-) multiple intestinal neoplasia mice developed significantly fewer tumors than Ccnd1(+/-) or Ccnd1(+/+) mice (P = 0.003). We conclude that cyclin D1 is not essential for intestinal tumorigenesis, but it may act as a modifier gene.

Type

Journal article

Journal

Cancer research

Publication Date

08/2002

Volume

62

Pages

4562 - 4565

Addresses

Cancer and Immunogenetics Laboratory, Cancer Research UK, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom.

Keywords

Animals, Mice, Knockout, Mice, Intestinal Neoplasms, Disease Models, Animal, Cyclin D1, Cytoskeletal Proteins, Trans-Activators, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Gene Expression Regulation, Female, Male, beta Catenin, Transcriptional Activation