Poised epigenetic states and acquired drug resistance in cancer

被引：277

作者：

Brown, Robert ^{[1
]}

Curry, Edward ^{[1
]}

Magnani, Luca ^{[1
]}

Wilhelm-Benartzi, Charlotte S. ^{[1
]}

Borley, Jane ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Dept Surg & Canc, London W12 ONN, England

来源：

NATURE REVIEWS CANCER | 2014年 / 14卷 / 11期

关键词：

MGMT PROMOTER METHYLATION; OVARIAN-CANCER; PHASE-II; CISPLATIN RESISTANCE; TEMOZOLOMIDE RESISTANCE; DNA HYPERMETHYLATION; TUMOR HETEROGENEITY; CELL SIGNATURE; STEM-CELLS; P53; GENE;

D O I：

10.1038/nrc3819

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Epigenetic events, which are somatically inherited through cell division, are potential drivers of acquired drug resistance in cancer. The high rate of epigenetic change in tumours generates diversity in gene expression patterns that can rapidly evolve through drug selection during treatment, leading to the development of acquired resistance. This will potentially confound stratified chemotherapy decisions that are solely based on mutation biomarkers. Poised epigenetic states in tumour cells may drive multistep epigenetic fixation of gene expression during the acquisition of drug resistance, which has implications for clinical strategies to prevent the emergence of drug resistance.

引用

页码：747 / 753

页数：7

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