Abstract
Gene silencing through de novo methylation of CpG island promoters contributes to cancer. We find that Mbd2, which recruits co-repressor complexes to methylated DNA, is essential for efficient tumorigenesis in the mouse intestine. As Mbd2-deficient mice are viable and fertile, their resistance to intestinal cancer may be of therapeutic relevance.
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Acknowledgements
We thank K. Wilson, N. Hill and D. Scarborough for technical assistance. This work was funded by the Wellcome Trust and Cancer Research UK. J.B. is supported by the European Union. A.R.C. is a Royal Society Research Fellow.
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Sansom, O., Berger, J., Bishop, S. et al. Deficiency of Mbd2 suppresses intestinal tumorigenesis. Nat Genet 34, 145–147 (2003). https://doi.org/10.1038/ng1155
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DOI: https://doi.org/10.1038/ng1155
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