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Deficiency of Mbd2 suppresses intestinal tumorigenesis

Nature Genetics volume 34, pages 145–147 (2003)Cite this article

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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Figure 1: Deficiency of Mbd2 increases lifespan of ApcMin/+ mice in a dose-dependent manner.
Figure 2: Tumors of Mbd2−/− mice have lower incidence, are smaller in size and have an altered intestinal distribution.

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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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Authors and Affiliations

  1. Cardiff School of Biosciences, Cardiff University, Cardiff, Wales, UK

    Owen J Sansom, Stefan M Bishop & Alan R Clarke

  2. Wellcome Trust Centre for Cell Biology, Kings Buildings, Edinburgh University, Edinburgh, EH9 3JR, UK

    Jennifer Berger, Brian Hendrich & Adrian Bird

Authors
  1. Owen J Sansom
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  2. Jennifer Berger
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  3. Stefan M Bishop
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  4. Brian Hendrich
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  5. Adrian Bird
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  6. Alan R Clarke
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Correspondence to Adrian Bird.

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The authors declare no competing financial interests.

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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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