For patients who exhaust all traditional cancer therapies, pinpointing new molecular targets for therapy requires that we examine not only the differences between their "normal" DNA and the mutated DNA of their tumor, but also other factors that influence how genes are expressed.
These "other factors" are proteins that chemically modify either the DNA — without altering the genetic code — or DNA-associated proteins that regulate gene transcription. Such gene modifiers and regulators are collectively known as epigenetic mechanisms, as they cause gene variation above and beyond changes in the DNA sequence.
Epigenetic mechanisms can be passed on when cells divide, so they have a long-term influence on how cells behave and contribute to the development of cancer and other diseases. Today, we can characterize the entire epigenomes of diseased cells from individual patients by monitoring the genome-wide distribution of epigenetic marks, along with their "writers," "readers" and "erasers."
This capability, together with a rapidly increasing list of compounds and drugs that target epigenetic mechanisms, is moving us closer to more widely using epigenomics for personalizing both diagnostics and treatments. Better understanding epigenomics and related technologies and applying them to patient care is central to the work of the Epigenomics Program.