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靶向卵巢癌的表观基因组。

Targeting the epigenome in ovarian cancer.

机构信息

Department of Obstetrics & Gynecology, Division of Gynecologic Oncology, Duke University Medical Center, PO Box 91012, Durham, NC 27708, USA.

出版信息

Future Oncol. 2012 Feb;8(2):151-64. doi: 10.2217/fon.11.152.

DOI:10.2217/fon.11.152
PMID:22335580
Abstract

Epithelial ovarian cancer is the leading cause of death from gynecological cancers, largely owing to the development of recurrent intractable disease. Only a small number of distinct genetic mutations are known to contribute to ovarian carcinogenesis. Furthermore, understanding mechanistic genotype-phenotype links is complicated by frequent aneuploidy. Epigenetic deregulation is even more prominent, and ovarian cancers are replete with such aberrations that repress tumor suppressors and activate proto-oncogenes. Epigenetic therapies are emerging as promising agents for resensitizing platinum-resistant ovarian cancers. These drugs may also have the potential to alter epigenetic programming in cancer progenitor cells and provide a strategy for improving therapy of ovarian cancer.

摘要

上皮性卵巢癌是妇科癌症死亡的主要原因,主要是由于复发性难治性疾病的发展。只有少数明确的基因突变被认为与卵巢癌的发生有关。此外,由于经常出现非整倍体,理解机制基因型-表型联系变得更加复杂。表观遗传失调更为突出,卵巢癌中存在大量抑制肿瘤抑制因子和激活原癌基因的异常。表观遗传治疗作为重新敏感铂耐药卵巢癌的有前途的药物正在出现。这些药物也有可能改变癌症祖细胞中的表观遗传编程,并为改善卵巢癌的治疗提供一种策略。

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Genomic map of candidate human imprint control regions: the imprintome.人类候选印记控制区域的基因组图谱:印记组。
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Early Loss of Histone H2B Monoubiquitylation Alters Chromatin Accessibility and Activates Key Immune Pathways That Facilitate Progression of Ovarian Cancer.
早期组蛋白 H2B 单泛素化的丧失改变了染色质的可及性,并激活了关键的免疫途径,从而促进了卵巢癌的进展。
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Histones and their modifications in ovarian cancer - drivers of disease and therapeutic targets.卵巢癌中的组蛋白及其修饰物——疾病的驱动因素和治疗靶点。
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