Suppr超能文献

地西他滨

Decitabine.

作者信息

Daskalakis Michael, Blagitko-Dorfs Nadja, Hackanson Björn

机构信息

Division of Hematology and Oncology, Freiburg University Medical Center, Hugstetterstrasse 55, 79106, Freiburg, Germany.

出版信息

Recent Results Cancer Res. 2010;184:131-57. doi: 10.1007/978-3-642-01222-8_10.

Abstract

The pyrimidine analogs, 5-azacytidine (azacitidine, Vidaza) and its deoxy derivative, 5-aza-2'-deoxycytidine (decitabine, Dacogen, are the most widely used inhibitors of DNA methylation which trigger demethylation leading to a consecutive reactivation of epigenetically silenced tumor suppressor genes in vitro and in vivo. Although the antileukemic capacity of decitabine has been known for almost 40 years, its therapeutic potential in hematologic malignancies is still under intensive investigation. Multiple clinical trials have shown the promising activity of low-dose decitabine in AML, MDS, CML, and hemoglobinopathies, whereas its efficacy in solid tumors is rather limited.Clinical responses appear to be induced by both epigenetic alterations and the induction of cell-cycle arrest and/or apoptosis. Recent clinical trials have been investigating new dosing schedules, routes of administration, and combination of decitabine with other agents, including histone deacetylase (HDAC) inhibitors.

摘要

嘧啶类似物5-氮杂胞苷(阿扎胞苷,维达莎)及其脱氧衍生物5-氮杂-2'-脱氧胞苷(地西他滨,达珂)是最广泛使用的DNA甲基化抑制剂,它们能引发去甲基化,从而在体外和体内使表观遗传沉默的肿瘤抑制基因相继重新激活。尽管地西他滨的抗白血病能力已为人所知近40年,但其在血液系统恶性肿瘤中的治疗潜力仍在深入研究中。多项临床试验表明,低剂量地西他滨在急性髓系白血病(AML)、骨髓增生异常综合征(MDS)、慢性髓系白血病(CML)和血红蛋白病中具有有前景的活性,而其在实体瘤中的疗效相当有限。临床反应似乎是由表观遗传改变以及细胞周期阻滞和/或凋亡的诱导所引发的。最近的临床试验一直在研究地西他滨的新给药方案、给药途径以及与其他药物(包括组蛋白去乙酰化酶(HDAC)抑制剂)的联合应用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验