Abstract
Chromosomal rearrangements involving band 12p13 are found in a wide variety of human leukemias but are particularly common in childhood acute lymphoblastic leukemia. The genes involved in these rearrangements, however, have not been identified. We now report the cloning of a t(12;21) translocation breakpoint involving 12p13 and 21q22 in two cases of childhood pre-B acute lymphoblastic leukemia, in which t(12;21) rearrangements were not initially apparent. The consequence of the translocation is fusion of the helix-loop-helix domain of TEL, an ETS-like putative transcription factor, to the DNA-binding anti transactivation domains of the transcription factor AML1. These data show that TEL, previously shown to be fused to the platelet- derived growth factor receptor β in chronic myelomonocytic leukemia, can be implicated in the pathogenesis of leukemia through its fusion to either a receptor tyrosine kinase or a transcription factor. The TEL-AML1 fusion also indicates that translocations affecting the AML1 gene can be associated with lymphoid, as well as myeloid, malignancy.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 4917-4921 |
| Number of pages | 5 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 92 |
| Issue number | 11 |
| DOIs | |
| State | Published - May 23 1995 |
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Keywords
- ETS
- chromosome 12
- chromosome 21
- transcription factors
- translocation
ASJC Scopus subject areas
- General
Cite this
}
Fusion of the TEL gene on 12p13 to the AML1 gene on 21q22 in acute lymphoblastic leukemia. / Golub, Todd R.; Barker, George F.; Bohlander, Stefan K.; Hiebert, Scott W.; Ward, David C.; Bray-Ward, Patricia; Morgan, Elaine R; Raimondi, Susana C.; Rowley, Janet D.; Gilliland, D. Gary.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 92, No. 11, 23.05.1995, p. 4917-4921.Research output: Contribution to journal › Article
TY - JOUR
T1 - Fusion of the TEL gene on 12p13 to the AML1 gene on 21q22 in acute lymphoblastic leukemia
AU - Golub, Todd R.
AU - Barker, George F.
AU - Bohlander, Stefan K.
AU - Hiebert, Scott W.
AU - Ward, David C.
AU - Bray-Ward, Patricia
AU - Morgan, Elaine R
AU - Raimondi, Susana C.
AU - Rowley, Janet D.
AU - Gilliland, D. Gary
PY - 1995/5/23
Y1 - 1995/5/23
N2 - Chromosomal rearrangements involving band 12p13 are found in a wide variety of human leukemias but are particularly common in childhood acute lymphoblastic leukemia. The genes involved in these rearrangements, however, have not been identified. We now report the cloning of a t(12;21) translocation breakpoint involving 12p13 and 21q22 in two cases of childhood pre-B acute lymphoblastic leukemia, in which t(12;21) rearrangements were not initially apparent. The consequence of the translocation is fusion of the helix-loop-helix domain of TEL, an ETS-like putative transcription factor, to the DNA-binding anti transactivation domains of the transcription factor AML1. These data show that TEL, previously shown to be fused to the platelet- derived growth factor receptor β in chronic myelomonocytic leukemia, can be implicated in the pathogenesis of leukemia through its fusion to either a receptor tyrosine kinase or a transcription factor. The TEL-AML1 fusion also indicates that translocations affecting the AML1 gene can be associated with lymphoid, as well as myeloid, malignancy.
AB - Chromosomal rearrangements involving band 12p13 are found in a wide variety of human leukemias but are particularly common in childhood acute lymphoblastic leukemia. The genes involved in these rearrangements, however, have not been identified. We now report the cloning of a t(12;21) translocation breakpoint involving 12p13 and 21q22 in two cases of childhood pre-B acute lymphoblastic leukemia, in which t(12;21) rearrangements were not initially apparent. The consequence of the translocation is fusion of the helix-loop-helix domain of TEL, an ETS-like putative transcription factor, to the DNA-binding anti transactivation domains of the transcription factor AML1. These data show that TEL, previously shown to be fused to the platelet- derived growth factor receptor β in chronic myelomonocytic leukemia, can be implicated in the pathogenesis of leukemia through its fusion to either a receptor tyrosine kinase or a transcription factor. The TEL-AML1 fusion also indicates that translocations affecting the AML1 gene can be associated with lymphoid, as well as myeloid, malignancy.
KW - ETS
KW - chromosome 12
KW - chromosome 21
KW - transcription factors
KW - translocation
UR - http://www.scopus.com/inward/record.url?scp=0029004541&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029004541&partnerID=8YFLogxK
U2 - 10.1073/pnas.92.11.4917
DO - 10.1073/pnas.92.11.4917
M3 - Article
VL - 92
SP - 4917
EP - 4921
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 11
ER -