p14ARF,9p15INK4b and p16INK4a methylation status in chronic myelogenous leukemia
p14ARF,9p15INK4b and p16INK4a methylation status in chronic myelogenous leukemia
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DOI：
10.1080/10428190410001714025
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发表时间：
2004-10-01
影响因子：
2.6
通讯作者：
Roche, J
中科院分区：
文献类型：
--
作者：
Kusy, S;Larsen, CJ;Roche, J
蛋白质p15（INK4b）、p14（ARF）和p16（INK4a）的INK4家族作为细胞周期抑制剂起作用，其中它们参与抑制G1期进展。p15（INK4b）启动子的甲基化似乎从未发生在实体瘤中，但在血液恶性肿瘤中是一种主要的基因沉默机制。p14（ARF）和p16（INK4a）启动子甲基化通常发生在实体瘤中，但也发生在白血病和淋巴瘤中。在慢性粒细胞白血病（CML）中，只有少数报告已发表关于INK4甲基化和文献的结果是不一致的。因此，显然，更多的大型系列作品必须独立完成。
The INK4 family of proteins p15(INK4b), p14(ARF) and p16(INK4a) function as cell cycle inhibitors where they are involved in the inhibition of G1 phase progression. Methylation of the p15(INK4b) promoter never seems to occur in solid tumors but is a major gene silencing mechanism in hematological malignancies. p14(ARF) and p16(INK4a) promoter methylation often occurs in solid tumors but also in leukemias and lymphomas. In chronic myelogenous leukemia (CML), only a few reports have been published regarding INK4 methylation and the results of the literature are discordant. Thus clearly, more works on large series have to be performed independently.