The promise of epigenomic therapeutics in pancreatic cancer

被引:39
|
作者
Lomberk, Gwen A. [1 ,2 ,3 ]
Iovanna, Juan [4 ,5 ]
Urrutia, Raul [1 ,2 ,3 ]
机构
[1] Mayo Clin, Lab Epigenet & Chromatin Dynam, Gastroenterol Res Unit, Dept Biochem & Mol Biol, Rochester, MN USA
[2] Mayo Clin, Lab Epigenet & Chromatin Dynam, Gastroenterol Res Unit, Dept Biophys, Rochester, MN USA
[3] Mayo Clin, Lab Epigenet & Chromatin Dynam, Gastroenterol Res Unit, Dept Med, Rochester, MN USA
[4] Aix Marseille Univ, CRCM, INSERM, U1068,CNRS,UMR 7258, Parc Sci & Technol Luminy, Marseille, France
[5] Inst Paoli Calmettes, Parc Sci & Technol Luminy, Marseille, France
关键词
chromatin; DNA methylation; DNMTs; epigenetics; HATs; HDACs; HMTs; noncoding RNAs; pancreatic cancer; therapeutics; HISTONE DEACETYLASE INHIBITORS; DUCTAL ADENOCARCINOMA; DNA METHYLATION; FAMILY PROTEINS; MULTIPLE GENES; EXPRESSION; THERAPY; EPIGENETICS; METHYLTRANSFERASES; MECHANISMS;
D O I
10.2217/epi-2015-0016
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
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.
引用
收藏
页码:831 / 842
页数:12
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