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Abstract
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.
Financial & competing interests disclosure
The authors are supported by funding from the NIH (grants R01 CA178627 to GA Lomberk and R01 DK52913 to R Urrutia), the Mayo Foundation, as well as the Mayo Clinic Center for Cell Signaling in Gastroenterology (P30DK084567) and the Mayo Clinic SPORE in Pancreatic Cancer (P50 CA102701). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.