Epigenetic mechanisms such as DNA methylation and chromatin modification allow the propagation of defined cellular states without alterations in the coding capacity of DNA, e.g. during ontogeny. Severe disturbances of several epigenetic mechanisms are found in cancer, prominently in prostate carcinoma, the most frequent lethal cancer in elderly males. Alterations of DNA methylation comprise the coordinated hypermethylation of several genes at an early stage of prostate cancer development and decreased methylation of retrotransposon sequences in a subgroup of cases with more aggressive properties. These changes can be employed for the improved detection and classification of prostate cancer. In the last two years, our group has focused on two issues. First, we have followed up a specific hypothesis on an mutual interaction between chromatin regulators and DNA methylation: Certain genes active in early embryonic and germ cells regulate DNA methylation, chromatin structure and gene activity, but might in turn be themselves silenced by DNA methylation in differentiated somatic cells. Reactivation of such genes elicited by DNA methylation alterations might contribute to cancer development. Secondly, we are attempting to delineate the biological processes responsible for the more aggressive behavior of prostate cancers with retrotransposon hypomethylation.