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Epigenetics acts as a bridge between genetic predisposition and the actual expression of genes. But whereas the genetic information itself, contained in the DNA sequence of a gene, is quite fixed, its expression can be strongly varying.


There are molecular and chemical switches for the precise regulation of gene expression, activating or inactivating the genes of interest. Those switches can be of steric nature, such as the winding of DNA on histones, or due to chemical modifications such as the methylation of cytosines (see Fig. 1).


Alterations in DNA methylation patterns are among the earliest and most common events in tumourigenesis. In the mammalian genome, methylation takes place predominantly at cytosine bases that are located 5' to a guanosine in a CpG dinucleotide. While this dinucleotide is generally underrepresented in the whole genome, short genomic sequences are rich in the CpG pattern. Regions rich in the CpG pattern are known as CpG islands. These regions, which include many gene promoters, are made up of a few hundred or more nucleotides. Both global and regional hypermethylation have been described in human tumour cell lines and a wide spectrum of cancers. Hypomethylation or complete absence of methylation of CpG islands is typically associated with the activity of genes; in contrast hypermethylation of CpG islands within promoter regions has been correlated with decreased gene activity.


Epigenetic analysis provide insights into these regulatory effects of the genes. Thus, epigenetic research plays an important role in understanding diseases. It also opens new diagnostic and therapeutic pathways to meet the challenges of today’s health care systems.


In this context, our analytical services form the basis to detect, quantify and understand methylation of these regulated DNA regions.

Fig. 1: Regulation of gene expression on an epigenetic level by methylation. Primarily methylated genes cannot be translated or replicated and are therefore inactivated.