t(3;21)(q26;q22) with AML1 rearrangement in a de novo childhood acute monoblastic leukaemia

被引:14
作者
Johansson, B
Fioretos, T
Garwicz, S
Heim, S
Mitelman, F
机构
[1] UNIV LUND HOSP,DEPT PAEDIAT,S-22185 LUND,SWEDEN
[2] NORWEGIAN RADIUM HOSP,INST CANC RES,DEPT GENET,N-0310 MONTEBELLO,OSLO,NORWAY
关键词
childhood; acute leukaemia; translocation; AML1;
D O I
10.1046/j.1365-2141.1996.d01-1468.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
t(3;21)(q26;q22) is a recurrent chromosomal abnormality in Philadelphia-positive chronic myeloid leukaemia in blast crisis and in treatment-related myelodysplastic syndrome and acute myeloid leukaemia. The molecular consequences of the t(3;21) are presently being unravelled; various transcripts between the AML1 gene in 21q22 and several unrelated genes, i.e. EAP, EVI1 and MDS1, in 3q26 are generated, resulting in the formation of a chimaeric transcription factor. The t(3;21) has only rarely been described in de novo leukaemias and never before in an acute leukaemia in a child. We here present the clinical, cytogenetic and molecular genetic findings in a boy with a de novo acute monoblastic leukaemia with t(3;21)(q26;q22) and AML1 rearrangement.
引用
收藏
页码:429 / 431
页数:3
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