In addition to genetic information that is embedded in the DNA base sequence, there is a second code of life: chemical changes in DNA or in their packaging proteins, the histones, form an additional control level which determines which genes are actually read. This “epigenetic“ code has a decisive influence on all cellular processes – and therefore also on whether a cell develops into a cancer cell.
“The research projects that are concerned with the connection between epigenesis and cancer have become quite numerous. It's high time we provided a platform for this topic via regular conferences so that we can facilitate the exchange of ideas,“ says Christoph Plass from the German Cancer Research Center (DKFZ), one of the organizers of the event. His DKFZ colleague Karsten Rippe, also one of the organizers, adds: “The conference will from now on be held every two years and will cover the field in its entirety.“
A whole section of the conference is concerned with the question of how changes in the epigenetic code can disrupt the carefully balanced interplay of cellular signal pathways and therefore facilitate cancer growth. Joseph Costello from the University of San Francisco describes how genetic and epigenetic mutations develop almost in tandem and in close proximity to each other while brain tumors transition from benign to malignant, and eventually allow the cell to degenerate altogether.
The epigenetic programming is crucial to the identity of a cell. Frank Lyko of the DKFZ examines this point in his talk. He has discovered indications that various subtypes of colon cancer from different original cells originate in the intestinal mucosa. This could allow for the specific DNA-Methylation patterns of the cells to be used for the exact classification of colon tumors.
Toshikazu Ushijima of the National Cancer Research Institute in Tokyo sees epigenetic patterns as helpful biomarkers: With certain types of cancer, such as a neuroblastoma or stomach cancer, these patterns could be used to predict the further development of the illness.
In countless questions, cancer epigenesis has left basic research behind and scientists are already applying their knowledge into practical clinical applications. Stephen B. Baylin of the Johns Hopkin University School of Medicine, Baltimore, is one of the pioneers in this field. He reports various approaches of utilizing epigenetic changes in tumors as target structures for new cancer therapies. Other projects are already in the clinical test phase. Olaf Witt, of the DKFZ and Heidelberg University Hospital, has already reported completing a clinical study. It tested the efficacy of the epigenetically functioning medication Vorinostat on leukemia and solid tumors with children – the analysis of the trial will follow soon.
Journalists are cordially invited to attend the conference.