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

The majority of human colorectal cancers have elevated beta-catenin/TCF reg ulated 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 tumorigen esis in mice. Expression of CDX2 was found to be induced by restoring expre ssion of wild type APC in a colorectal cancer cell line. These findings rai se the intriguing possibility that CDX2 contributes to APC's tumor suppress ive effects.