The t(12;21) of acute lymphoblastic leukemia results in a tel-AML1 gene fusion.

@article{Romana1995TheTO,
  title={The t(12;21) of acute lymphoblastic leukemia results in a tel-AML1 gene fusion.},
  author={S. Romana and M. Mauchauff{\'e} and M. le Coniat and I. Chumakov and D. Le Paslier and R. Berger and O. Bernard},
  journal={Blood},
  year={1995},
  volume={85 12},
  pages={
          3662-70
        }
}
Analysis of a growing number of chromosomal translocations in human tumors have shown that they frequently result in gene fusions encoding chimeric proteins. We have characterized the recurrent t(12;21)(p12;q22) translocation present in human B-lineage acute leukemias. This translocation fused two genes, tel and AML1, that have previously been described in chromosomal translocations specific for myeloid malignancies. These two genes therefore belong to an increasing number of human genes that… Expand
High frequency of t(12;21) in childhood B-lineage acute lymphoblastic leukemia.
TLDR
It is reported that fusion of TEL to AML1 is specifically observed in at least 16% of the childhood B-lineage acute lymphoblastic leukemia investigated, none of which had been previously identified as harboring t(12;21). Expand
Detection of the Der (21)t(12;21) chromosome forming the TEL-AML1 fusion gene in childhood acute lymphoblastic leukemia.
TLDR
RT-PCR combined with FISH analysis of posttreatment samples appears to be useful in detecting early relapse or minimal residual disease and thus, is expected to optimize the treatment strategy for patients with t(12;21). Expand
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TLDR
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The 12;21 translocation involving TEL and deletion of the other TEL allele: two frequently associated alterations found in childhood acute lymphoblastic leukemia.
TLDR
The results indicate that the association between the t(12;21) and the deletion of the nontranslocated allele of TEL is among the most frequent abnormalities observed in B-lineage ALLs, and TEL as the actual target of 12p12-13 deletions in patients that associate a t( 12; 21) with a deletion. Expand
Occurrence of TEL-AML1 fusion resulting from (12;21) translocation in human early B-lineage leukemia cell lines
TLDR
The recurrent (12;21)(p13;q22) translocation fuses the two genes TEL and AML1 that have previously been cloned from translocation breakpoints in myeloid leukemias and provides a further example of the paradigm of TEL-AML1 fusion accompanied by deletion of the residual TEL allele. Expand
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TLDR
6 cell lines with the TEL-AMLl fusion transcript are described, showing the coexistence of multiple genetic defects in childhood B-lineage ALL and whether TEL inactivation has a role in leukemogenesis is currently unknown. Expand
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TLDR
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TLDR
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TLDR
The results show that the TEL-ARNT fusion protein is the crucial product of the translocation and suggest that interference with the activity of AhR or HIF1alpha can contribute to leukemogenesis. Expand
Characterization of additional genetic events in childhood acute lymphoblastic leukemia with TEL/AML1 gene fusion: a molecular cytogenetics study
TLDR
It is confirmed that additional or secondary genetic changes including AML1 amplification are commonly encountered in childhood ALL with TEL/AML1 gene fusion, which are envisaged to play significant roles in disease progression. Expand
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