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

Abstract:

: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.

journal_name

Br J Haematol

authors

Au WY,Fung AT,Ma ES,Chan CH,Wong KF,Chim CS,Liang RH,Kwong YL

doi

10.1111/j.1365-2141.2005.05818.x

subject

Has Abstract

pub_date

2005-12-01 00:00:00

pages

632-5

issue

5

eissn

0007-1048

issn

1365-2141

pii

BJH5818

journal_volume

131

pub_type

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