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

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

Research output: Contribution to journalArticle

Abstract

The majority of human colorectal cancers have elevated β-catenin/TCF regulated transcription due to either inactivating mutations of the APC tumor suppressor gene or activating mutations of β-catenin. Surprisingly, one commonly used colorectal cancer cell line was found to have intact APC and β-catenin and no demonstrable β-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.

Original languageEnglish (US)
Pages (from-to)5010-5014
Number of pages5
JournalOncogene
Volume18
Issue number35
DOIs
StatePublished - Sep 2 1999

Keywords

  • APC
  • CDX2
  • Colorectal cancer
  • Mutation
  • Regulation

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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    Da Costa, L. T., He, T. C., Yu, J., Sparks, A. B., Morin, P. J., Polyak, K., Laken, S., Vogelstein, B., & Kinzler, K. W. (1999). CDX2 is mutated in a colorectal cancer with normal APC/β-catenin signaling. Oncogene, 18(35), 5010-5014. https://doi.org/10.1038/sj.onc.1202872