CDX2 is mutated in a colorectal cancer with normal APC/β-catenin signaling View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1999-09

AUTHORS

Luis T da Costa, Tong-Chuan He, Jian Yu, Andrew B Sparks, Patrice J Morin, Kornelia Polyak, Steve Laken, Bert Vogelstein, Kenneth W Kinzler

ABSTRACT

The majority of human colorectal cancers have elevated beta-catenin/TCF regulated transcription due to either inactivating mutations of the APC tumor suppressor gene or activating mutations of beta-catenin. Surprisingly, one commonly used colorectal cancer cell line was found to have intact APC and beta-catenin and no demonstrable beta-catenin/TCF regulated transcription. However, this line did possess a truncating mutation in one allele of CDX2, a gene whose inactivation has recently been shown to cause colon tumorigenesis in mice. Expression of CDX2 was found to be induced by restoring expression of wild type APC in a colorectal cancer cell line. These findings raise the intriguing possibility that CDX2 contributes to APC's tumor suppressive effects. More... »

PAGES

5010

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1202872

DOI

http://dx.doi.org/10.1038/sj.onc.1202872

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1006228955

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10490837


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