Serial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxide

被引：7

作者：

Au, WY

Fung, AT

Ma, ES

Chan, CH

Wong, KF

Chim, CS

Liang, RH

Kwong, YL

机构：

[1] Univ Hong Kong, Dept Med, Hong Kong, Hong Kong, Peoples R China

[2] Univ Hong Kong, Dept Pathol, Hong Kong, Hong Kong, Peoples R China

[3] Queen Elizabeth Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China

[4] Queen Elizabeth Hosp, Dept Pathol, Hong Kong, Hong Kong, Peoples R China

来源：

BRITISH JOURNAL OF HAEMATOLOGY | 2005年 / 131卷 / 05期

关键词：

acute promyelocytic leukaemia; CDKN2B; CDKN2A; methylation;

D O I：

10.1111/j.1365-2141.2005.05818.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

收藏

页码：632 / 635

页数：4

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