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, Kathleen Richkind

Research output: Contribution to journalArticle

33 Scopus citations

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 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.

Original languageEnglish (US)
Pages (from-to)2168-2170
Number of pages3
JournalBlood
Volume97
Issue number7
DOIs
StatePublished - Apr 1 2001
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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