Pancreatic ductal adenocarcinoma (PDAC) is often viewed to arise primarily by genetic alterations. However, today we know that many aspects of the cancer phenotype require a crosstalk among these genetic alterations with epigenetic changes. Indeed, aberrant gene expression patterns, driven by epigenetics are fixed by altered signaling from mutated oncogenes and tumor suppressors to define the PDAC phenotype. This conceptual framework may have significant mechanistic value and could offer novel possibilities for treating patients affected with PDAC. In fact, extensive investigations are leading to the development of small molecule drugs that reversibly modify the epigenome. These new 'epigenetic therapeutics' discussed herein are promising to fuel a new era of studies, by providing the medical community with new tools to treat this dismal disease.
Keywords: DNA methylation; DNMTs; HATs; HDACs; HMTs; chromatin; epigenetics; noncoding RNAs; pancreatic cancer; therapeutics.