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DNA甲基化与卡波西肉瘤的研究进展 被引量：1

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摘要 DNA甲基化是很多恶性肿瘤的发病机制。甲基化能够导致抑癌基因的表达沉默,使正常细胞的生长分化调控失常以及DNA损伤不能及时修复,导致肿瘤形成。近年研究表明,Kaposi肉瘤(KS)的形成与TβRⅡ基因(转化生长因子Ⅱ型受体基因)、p16IN K4A基因、Axl基因(受体酪氨酸激酶基因)发生甲基化有关。另外,甲基化是个可逆过程,5-氮-2'-脱氧胞苷(5-aza-CdR)能够使表达沉默的抑癌基因重新激活,有可能成为KS治疗的一个新途径。
作者 邹云敏 普雄明
机构地区 石河子大学医学院 新疆维吾尔自治区人民医院皮肤性病科
出处 《中国麻风皮肤病杂志》 2012年第2期104-106,共3页 China Journal of Leprosy and Skin Diseases
基金 新疆维吾尔自治区自然科学基金资助(2009211A24)
关键词 KAPOSI肉瘤 甲基化 基因
分类号 R739.5 [医药卫生—肿瘤]
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参考文献12

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中国麻风皮肤病杂志
2012年 第2期

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