The highly coordinated activities of epigenetic regulators, such as histone acetyltransferases (HATs)*, methyltransferases, and chromatin-remodeling enzymes, are essential for controlling and maintaining normal gene expression patterns in humans. Deregulation of these epigenetic regulators, however, results in aberrant gene expression consequently leading to cancer and other diseases. Thus, in the past decade it has become increasingly clear that the heritable alterations in cancer cells occur not only at the level of the primary DNA sequence but also at the level of the cancer epigenome. As we advance our understanding of how alterations in specific epigenetic regulators lead to malignant cellular transformation, increasing efforts have been put forth to identify drugs that may inhibit the aberrant activities of these epigenetic regulators with the hopes of reversing the disease state. Indeed, anticancer drugs targeting DNA methyltransferases and histone deacetylases (HDACs)* have successfully demonstrated antitumor activity in the clinic, as exemplified by the HDAC inhibitor Vorinostat approved by the FDA in 2006. More recently reports on the roles of the bromodomain-containing BET family members and methyltransferase EZH2 in driving cell growth and survival have provided further validation of epigenetic regulators as critical drivers of the transformed cancer cell phenotype. In this symposium, we will review the advances made in understanding the roles of epigenetic regulators in cancer development and the progresses towards designing effective treatments targeting the epigenome.
*Reception to follow.
|Nonmember (Student / Postdoc / Resident / Fellow)
Mission Partner support for the Frontiers of Science program provided by