Cancer Epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance

被引：834

作者：

Easwaran, Hariharan ^{[1
]}

Tsai, Hsing-Chen ^{[1
]}

Baylin, Stephen B. ^{[1
]}

机构：

[1] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD 21287 USA

来源：

MOLECULAR CELL | 2014年 / 54卷 / 05期

基金：

美国国家卫生研究院;

关键词：

ISLAND METHYLATOR PHENOTYPE; INTRAGENIC DNA METHYLATION; PROMOTER HYPERMETHYLATION; CLONAL EVOLUTION; GENOMIC ANALYSIS; GENE-EXPRESSION; CELL SIGNATURE; IDH2; MUTATIONS; FIELD; MECHANISMS;

D O I：

10.1016/j.molcel.2014.05.015

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The existence of subpopulations of cells in cancers with increased tumor-initiating capacities and self-renewal potential, often termed "cancer stem cells," is a much discussed and key area of cancer biology. Such cellular heterogeneity is very important because of its impact on therapy and especially states of treatment resistance. A major question is whether there is plasticity for evolution of these cell states during tumorigenesis that can involve movement between cell populations in a reversible fashion. In this review, we discuss the possible role of epigenetic abnormalities as well as genetic alterations in such dynamics and in the creation of cellular heterogeneity in cancers of all types.

引用

页码：716 / 727

页数：12

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