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

Johansson, Bertil LU ; Fioretos, Thoas LU ; Garwicz, Stanislaw LU ; Heim, Sverre LU and Mitelman, Felix LU (1996) In British Journal of Haematology 92(2). p.429-431
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
childhood, acute leukaemia, translocation, AML1
in
British Journal of Haematology
volume
92
issue
2
pages
429 - 431
publisher
Federation of European Neuroscience Societies and Blackwell Publishing Ltd
external identifiers
  • pmid:8603012
  • scopus:0030032110
ISSN
0007-1048
DOI
10.1046/j.1365-2141.1996.d01-1468.x
language
English
LU publication?
yes
id
1fad697c-735b-4c00-9e38-132038dbdd43 (old id 1110598)
date added to LUP
2008-07-24 09:20:23
date last changed
2017-01-01 05:03:38
@article{1fad697c-735b-4c00-9e38-132038dbdd43,
  abstract     = {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.},
  author       = {Johansson, Bertil and Fioretos, Thoas and Garwicz, Stanislaw and Heim, Sverre and Mitelman, Felix},
  issn         = {0007-1048},
  keyword      = {childhood,acute leukaemia,translocation,AML1},
  language     = {eng},
  number       = {2},
  pages        = {429--431},
  publisher    = {Federation of European Neuroscience Societies and Blackwell Publishing Ltd},
  series       = {British Journal of Haematology},
  title        = {t(3;21)(q26;q22) with AML1 rearrangement in a de novo childhood acute monoblastic leukaemia},
  url          = {http://dx.doi.org/10.1046/j.1365-2141.1996.d01-1468.x},
  volume       = {92},
  year         = {1996},
}