Literature DB >> 7533526

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.

N Sacchi1, P E Nisson, P C Watkins, F Faustinella, J Wijsman, A Hagemeijer.   

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.

Entities:  

Mesh:

Substances:

Year:  1994        PMID: 7533526     DOI: 10.1002/gcc.2870110405

Source DB:  PubMed          Journal:  Genes Chromosomes Cancer        ISSN: 1045-2257            Impact factor:   5.006


  6 in total

1.  The t(12;21) translocation converts AML-1B from an activator to a repressor of transcription.

Authors:  S W Hiebert; W Sun; J N Davis; T Golub; S Shurtleff; A Buijs; J R Downing; G Grosveld; M F Roussell; D G Gilliland; N Lenny; S Meyers
Journal:  Mol Cell Biol       Date:  1996-04       Impact factor: 4.272

2.  Expression of the human acute myeloid leukemia gene AML1 is regulated by two promoter regions.

Authors:  M C Ghozi; Y Bernstein; V Negreanu; D Levanon; Y Groner
Journal:  Proc Natl Acad Sci U S A       Date:  1996-03-05       Impact factor: 11.205

Review 3.  Transcriptional regulation during myelopoiesis.

Authors:  N Lenny; J J Westendorf; S W Hiebert
Journal:  Mol Biol Rep       Date:  1997-08       Impact factor: 2.316

4.  The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation.

Authors:  J J Westendorf; C M Yamamoto; N Lenny; J R Downing; M E Selsted; S W Hiebert
Journal:  Mol Cell Biol       Date:  1998-01       Impact factor: 4.272

5.  The chimeric genes AML1/MDS1 and AML1/EAP inhibit AML1B activation at the CSF1R promoter, but only AML1/MDS1 has tumor-promoter properties.

Authors:  C S Zent; C Mathieu; D F Claxton; D E Zhang; D G Tenen; J D Rowley; G Nucifora
Journal:  Proc Natl Acad Sci U S A       Date:  1996-02-06       Impact factor: 11.205

6.  Control of alternative splicing by forskolin through hnRNP K during neuronal differentiation.

Authors:  Wenguang Cao; Aleh Razanau; Dairong Feng; Vincent G Lobo; Jiuyong Xie
Journal:  Nucleic Acids Res       Date:  2012-06-08       Impact factor: 16.971

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.