【摘要】：正阿扎胞苷(azacitidine)于2004-05-19被美國食品藥品監(jiān)督管理局(FDA)批準上市,是第一個被批準用于骨髓增生異常綜合征(MDS)的表觀遺傳學修飾治療藥物。近年發(fā)現(xiàn),DNA過度甲基化(hypermethylation)可使包括p15INK4b、p21、CALC1、E-cadherin、HIC-1、RASSFIA等多種調(diào)控正常細胞生長、分化及凋亡的基因表達受到抑制,從而導致MDS的發(fā)病。因此,DNA的去甲基化治療已經(jīng)成為MDS的一個重要治療靶點[1]。作為一種胞嘧啶核苷類似物,阿扎胞苷在DNA復制時可與DNA甲基轉(zhuǎn)移酶(DNMT)競爭性結(jié)合,抑制細胞中新合成DNA的甲基化,從而恢復多種與細胞增殖
[Abstract]:Azacytidine (azacitidine) was approved by the Food and Drug Administration (FDA) (FDA) on May 19, 2004. It is the first epigenetic modification drug approved for (MDS) in myelodysplastic syndrome (MDS). In recent years, it has been found that DNA hypermethylation of (hypermethylation) can inhibit the expression of many genes regulating the growth, differentiation and apoptosis of normal cells, including p15INK4bP21CALC1HIC-1RASSFIA, which may lead to the pathogenesis of MDS. Therefore, demethylation of DNA has become an important therapeutic target for MDS [1]. As a cytosine nucleoside analogue, azacytidine can competitively bind to DNA methyltransferase (DNMT) during DNA replication, inhibiting the methylation of newly synthesized DNA in cells, thus restoring multiple cell proliferation.
【作者單位】： 北京大學人民醫(yī)院風濕免疫科;北京大學人民醫(yī)院呼吸內(nèi)科;
【分類號】：R563
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本文編號：2382417