Abstract
Epigenetic aberrations such as global hypomethylation and gene-specific hypermethylation are key events that underlie tumour development. Such scenarios are brought about by the loss of control of methylation patterns which typically are reversed in neoplasia in comparison to normal states. Despite the methylation process being termed epigenetic, suggesting that it is not a heritable condition, there is strong evidence in mouse models suggesting that epimutations within the germline may provide a mechanism through which methylation variations can be transmissible to offspring. The first half of the review will focus on the nature of methylation-induced gene silencing and transmission of this information through the germline. The latter half will focus on the cause of aberrant DNA methylation.