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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