Epigenetic Determinants of Cancer

被引：886

作者：

Baylin, Stephen B. ^{[1
]}

Jones, Peter A. ^{[2
]}

机构：

[1] Johns Hopkins Univ, Sch Med, Canc Biol Program, Baltimore, MD 21287 USA

[2] Van Andel Res Inst, Grand Rapids, MI 49503 USA

来源：

COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY | 2016年 / 8卷 / 09期

关键词：

TUMOR-SUPPRESSOR GENE; HISTONE DEACETYLASE INHIBITION; ISLAND METHYLATOR PHENOTYPE; ACUTE MYELOID-LEUKEMIA; RANDOMIZED PHASE-II; CELL LUNG-CANCER; DNA METHYLATION; MYELODYSPLASTIC SYNDROME; CPG ISLAND; PROMOTER HYPERMETHYLATION;

D O I：

10.1101/cshperspect.a019505

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Epigenetic changes are present in all human cancers and are now known to cooperate with genetic alterations to drive the cancer phenotype. These changes involve DNA methylation, histone modifiers and readers, chromatin remodelers, microRNAs, and other components of chromatin. Cancer genetics and epigenetics are inextricably linked in generating the malignant phenotype; epigenetic changes can cause mutations in genes, and, conversely, mutations are frequently observed in genes that modify the epigenome. Epigenetic therapies, in which the goal is to reverse these changes, are now one standard of care for a preleukemic disorder and form of lymphoma. The application of epigenetic therapies in the treatment of solid tumors is also emerging as a viable therapeutic route.

引用

页数：35

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