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AML1 fusion transcripts in t(3;21) positive leukemia: evidence of molecular heterogeneity and usage of splicing sites frequently involved in the generation of normal AML1 transcripts.
- Source :
-
Genes, chromosomes & cancer [Genes Chromosomes Cancer] 1994 Dec; Vol. 11 (4), pp. 226-36. - Publication Year :
- 1994
-
Abstract
- The t(3;21)(q26;q22) is associated with chronic myelogenous leukemia in blast crisis (CML-BC), leukemia evolving from (therapy-related) myelodysplasia, and with leukemia following other hematopoietic proliferative diseases. Molecular cytogenetic analysis and cloning of a few t(3;21) cases indicate that the breakpoints are quite heterogeneous even within a specific clinical phenotype. Interestingly some of the (3;21) breakpoints involve the AML1 gene previously found rearranged in the t(8;21) associated with acute myelogenous leukemia. AML1 is related to the Drosophila gene runt and is the human counterpart of the gene for the alpha subunit of the nuclear polyoma enhancer binding protein (PEBP2) also known as the core binding factor (CBF). In the t(3;21) AML1 was found rearranged with EAP, a gene on chromosome 3 encoding a small ribosomal protein, as well as with EV11, another gene on chromosome 3. Here we report our study of six cases of t(3;21). By using fluorescence in situ hybridization (FISH) analysis and AML1 probes we could conclude that at least in two CML-BC cases the breakpoint occurred in the AML1 intron that is disrupted by the t(8;21). An AML1/EAP fusion transcript, different from the one described in a therapy-related myelodysplasia, was detected in both CML-BC cases. This transcript is expected to result in a predicted protein containing the AML1 nuclear binding domain with an attached stretch of 17 amino acids unrelated to the EAP small ribosomal protein. In the other t(3;21) patients we could not detect an AML1/EAP transcript or an AML1/EV11 transcript. This result suggests heterogeneity of the t(3;21) at the molecular level. The AML1 chimeric transcripts identified so far, both in the t(3;21) and in the t(8;21), diverge from the normal transcripts either after exon 5 or exon 6. Here we show that in normal AML1 transcripts different splicing events are seen to occur after AML1 exon 5 as well as exon 6.
- Subjects :
- Amino Acid Sequence
Base Sequence
Blast Crisis pathology
Chromosome Banding
Chromosomes, Human, Pair 21
Chromosomes, Human, Pair 3
Cloning, Molecular
Core Binding Factor Alpha 2 Subunit
DNA Probes
Exons
Humans
In Situ Hybridization, Fluorescence
Karyotyping
Leukemia, Myelogenous, Chronic, BCR-ABL Positive pathology
Leukemia, Myeloid, Acute pathology
Molecular Sequence Data
Neoplasm Proteins chemistry
RNA, Messenger genetics
Recombinant Fusion Proteins chemistry
Recombinant Fusion Proteins genetics
Blast Crisis genetics
DNA-Binding Proteins
Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics
Leukemia, Myeloid, Acute genetics
Neoplasm Proteins genetics
Proto-Oncogene Proteins
RNA Splicing
Transcription Factors
Translocation, Genetic
Subjects
Details
- Language :
- English
- ISSN :
- 1045-2257
- Volume :
- 11
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Genes, chromosomes & cancer
- Publication Type :
- Academic Journal
- Accession number :
- 7533526
- Full Text :
- https://doi.org/10.1002/gcc.2870110405