Abstract
An understanding of epigenetic drivers of tumorigenesis has developed rapidly during the last years. The identification of these changes including DNA methylation and histone modifications in gastroenteropancreatic neuroendocrine tumours (GEP-NETs) is a step forward in trying to define underlying biologic processes in this heterogeneous disease. The reversible nature of these changes represents a potential therapeutic target. We present an overview of the current knowledge of epigenetic alterations related to GEP-NETs, focusing on the influence and impact these changes have on pathogenesis and prognosis. The potential role of demethylating agents in the management of this patient population is discussed.
MeSH terms
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Chromatin Assembly and Disassembly
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CpG Islands
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DNA (Cytosine-5-)-Methyltransferase 1
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DNA (Cytosine-5-)-Methyltransferases / antagonists & inhibitors
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DNA Methylation
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Epigenesis, Genetic*
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Gastrointestinal Neoplasms / drug therapy
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Gastrointestinal Neoplasms / genetics*
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Genes, p16
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Histone Deacetylase Inhibitors / therapeutic use
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Humans
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MicroRNAs / physiology
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Neuroendocrine Tumors / drug therapy
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Neuroendocrine Tumors / genetics*
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Pancreatic Neoplasms / drug therapy
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Pancreatic Neoplasms / genetics*
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Promoter Regions, Genetic
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Tumor Suppressor Proteins / genetics
Substances
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Histone Deacetylase Inhibitors
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MicroRNAs
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RASSF1 protein, human
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Tumor Suppressor Proteins
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DNA (Cytosine-5-)-Methyltransferase 1
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DNA (Cytosine-5-)-Methyltransferases