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Blood, 1 April 2001, Vol. 97, No. 7, pp. 2168-2170

BRIEF REPORT

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

Robert Hromas, Tracey Busse, Audra Carroll, David Mack, Rinah Shopnick, Dong-Er Zhang, Harikrishna Nakshatri, and Kathleen Richkind

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.

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 AML1 gene 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.

© 2001 by The American Society of Hematology.
 

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