Abstract
The recurrent t(12;21)(p12;q22) translocation fuses two genes, TEL and AML1, that have previously been shown to be independently involved in myeloid malignant proliferations. A search for rearrangement of the TEL locus in the region known to be involved in t(12;21) was performed by Southern blotting in a panel of hematopoietic malignancies. The presence of a t(12;21) was confirmed by fluorescence in situ hybridization (FISH) and/or reverse transcriptase (RT)-polymerase chain reaction (PCR). We report that fusion of TEL to AML1 is specifically observed in at least 16% of the childhood B-lineage acute lymphoblastic leukemia (ALL) investigated, none of which had been previously identified as harboring t(12;21).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Base Sequence
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Blotting, Southern
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Burkitt Lymphoma / genetics*
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Child
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Child, Preschool
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Chromosomes, Human, Pair 12* / genetics
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Chromosomes, Human, Pair 21* / genetics
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Cloning, Molecular
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Core Binding Factor Alpha 2 Subunit
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DNA Primers / genetics
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DNA, Complementary / genetics
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DNA-Binding Proteins / genetics
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ETS Translocation Variant 6 Protein
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Female
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Gene Rearrangement
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Humans
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In Situ Hybridization, Fluorescence
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Male
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Molecular Sequence Data
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Neoplasm Proteins / genetics
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Polymerase Chain Reaction
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Proto-Oncogene Proteins c-ets
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Proto-Oncogene Proteins*
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Repressor Proteins*
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Transcription Factors / genetics
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Translocation, Genetic*
Substances
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Core Binding Factor Alpha 2 Subunit
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DNA Primers
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DNA, Complementary
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DNA-Binding Proteins
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Neoplasm Proteins
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-ets
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RUNX1 protein, human
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Repressor Proteins
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Transcription Factors