Fusion AML1 transcript in a radiation-associated leukemia results in a truncated inhibitory AML1 protein

Author:

Hromas Robert1,Busse Tracey1,Carroll Audra1,Mack David1,Shopnick Rinah1,Zhang Dong-Er1,Nakshatri Harikrishna1,Richkind Kathleen1

Affiliation:

1. From the Indiana University Cancer Center, Indianapolis, Indiana; Cancer Care Consultants, Las Vegas, Nevada; Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, California; and Genzyme Genetics, Santa Fe, New Mexico.

Abstract

Abstract AML1 is a transcription factor that is essential for normal hematopoietic development. It is the most frequent target for translocations in acute leukemia. Recently, fluorescence in situ hybridization was used to identify a novel syndrome of radiation-associated secondary acute myelogenous leukemia that had AML1 translocations. Using polymerase chain reaction, the AML1 fusion transcript was isolated from the patient who had a t(19;21) radiation-associated leukemia. The AML1gene is fused out of frame to chromosome 19 sequences, resulting in a truncated AML protein bearing the DNA binding domain but not the transcriptional activation domain. This fusion AML1 protein functions as an inhibitor of the normal AML1 protein.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference12 articles.

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