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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1110598
- author
- Johansson, Bertil
LU
; Fioretos, Thoas
LU
; Garwicz, Stanislaw
LU
; Heim, Sverre
LU
and Mitelman, Felix
LU
- organization
- publishing date
- 1996
- 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
- Wiley-Blackwell
- 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
- 2016-04-01 12:20:37
- date last changed
- 2022-01-27 02:18:51
@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}},
keywords = {{childhood; acute leukaemia; translocation; AML1}},
language = {{eng}},
number = {{2}},
pages = {{429--431}},
publisher = {{Wiley-Blackwell}},
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}},
doi = {{10.1046/j.1365-2141.1996.d01-1468.x}},
volume = {{92}},
year = {{1996}},
}