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MBD2 deficiency does not accelerate p53 mediated lymphomagenesis

Oncogene volume 24, pages 2430–2432 (2005)Cite this article

Abstract

Recent studies using hypomorphic DNA methyltransferase 1 (DNMT1) alleles have suggested that strategies aiming to reduce DNA methylation may increase genomic instability and lymphomagenesis. Given our recent finding that loss of methyl-binding domain protein 2 (Mbd2) suppresses intestinal tumorigenesis, we have tested whether loss of Mbd2 increases lymphomagenesis by intercrossing Mbd2 deficient mice with p53 deficient and p53 heterozygous mice. Unlike DNMT1, loss of Mbd2 does not accelerate lymphomagenesis, arguing that MBD2 may represent a better potential therapeutic target than DNMT1.

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Acknowledgements

This work was supported by CR-UK and the Wales Gene Park.

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Authors and Affiliations

  1. Mammalian Genetics, Cardiff School of Biosciences, University of Cardiff, Museum Avenue, PO Box 911, Cardiff, CF10 3US, UK

    Owen James Sansom, Stefan Mark Bishop & Alan Richard Clarke

  2. The Wellcome Trust Centre for Cell Biology, ICMB, University of Edinburgh, Edinburgh, EH9 3JR, UK

    Adrian Bird

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  1. Owen James Sansom
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  2. Stefan Mark Bishop
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  3. Adrian Bird
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  4. Alan Richard Clarke
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Correspondence to Alan Richard Clarke.

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Sansom, O., Bishop, S., Bird, A. et al. MBD2 deficiency does not accelerate p53 mediated lymphomagenesis. Oncogene 24, 2430–2432 (2005). https://doi.org/10.1038/sj.onc.1208166

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