Abstract

Pancreatic cancer remains among the deadliest forms of cancer with a 5 year survival rate less than 10%. With increasing numbers being observed, there is an urgent need to elucidate the pathogenesis of pancreatic cancer. While both contribute to disease progression, neither genetic nor environmental factors completely explain susceptibility or pathogenesis. Defining the links between genetic and environmental events represents an opportunity to understand the pathogenesis of pancreatic cancer. Epigenetics, the study of mitotically heritable changes in genome function without a change in nucleotide sequence, is an emerging field of research in pancreatic cancer. The main epigenetic mechanisms include DNA methylation, histone modifications and RNA interference, all of which are altered by changes to the environment. Epigenetic mechanisms are being investigated to clarify the underlying pathogenesis of pancreatic cancer including an increasing number of studies examining the role as possible diagnostic and prognostic biomarkers. These mechanisms also provide targets for promising new therapeutic approaches for this devastating malignancy.

Highlights

  • Schulze Center for Novel Therapeutics, Division of Oncology Research, Department of Oncology, Department of Gastroenterology, Ankara University School of Medicine, School of Medicine, 06100 Ankara, Turkey

  • The main epigenetic mechanisms can be grouped into three main categories—DNA methylation, modifications to core histone proteins comprising the nucleosome and RNA interference

  • Hank and Liss review these basic epigenetics mechanisms in pancreatic cancer. They summarize basic epigenetic mechanisms that pertain to pancreatic cancer, including histone acetylation and deacetylation models, histone methylation and bromodomain and extraterminal (BET) regulation

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Summary

Introduction

The main epigenetic mechanisms can be grouped into three main categories—DNA methylation, modifications to core histone proteins comprising the nucleosome and RNA interference. Recent advances in epigenetic mechanisms that control pancreatic carcinogenesis and the potential for targeting these mechanisms for diagnostic or therapeutic purposes will be discussed. This issue includes reviews on the role of the nuclear structure and nutriepigenomics in pancreatic cancer. Authors provide insight regarding potential therapeutic opportunities in targeting epigenetic mechanisms.

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