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 journalArticlepeer-review

119 Scopus citations


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
Issue number35
StatePublished - Sep 2 1999


  • APC
  • CDX2
  • Colorectal cancer
  • Mutation
  • Regulation

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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