Serial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxide
Serial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxide
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DOI：
10.1111/j.1365-2141.2005.05818.x
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发表时间：
2005-12-01
影响因子：
6.5
通讯作者：
Kwong, YL
中科院分区：
文献类型：
--
作者：
Au, WY;Fung, AT;Kwong, YL
研究了连续 90 名急性早幼粒细胞白血病患者的 CDKN2B（别名 p15）和 CDKN2A（别名 p16）启动子甲基化在疾病复发和进展中的情况。 CDKN2B 甲基化在首次复发时 (30/36, 83%) 明显高于就诊时 (48/77, 62%) (P = 0.025)，而 CDKN2A 甲基化似乎不受影响。 CDKN2B 甲基化的获得和丧失均发生在复发时，且获得更为频繁。在更晚期的复发中，CDKN2B 和 CDKN2A 甲基化没有显着增加。在第一次或随后的复发时，由于三氧化二砷的高效挽救，CDKN2B甲基化不会影响无事件生存或总生存。
Ninety consecutive patients with acute promyelocytic leukaemia were investigated for promoter methylation of CDKN2B (alias p15) and CDKN2A (alias p16) in disease relapse and progression. CDKN2B methylation was significantly more frequent at first relapse (30/36, 83%) than at presentation (48/77, 62%) (P = 0.025), while CDKN2A methylation appeared unaffected. Both acquisition and loss of CDKN2B methylation happened at relapse, with acquisition more frequent. No significant increase in CDKN2B and CDKN2A methylation occurred at more advanced relapses. At first or subsequent relapses, owing to highly effective salvage by arsenic trioxide, CDKN2B methylation did not impact on event-free survival or overall survival.