A novel syndrome of radiation-associated acute myeloid leukemia involving AML1 gene translocations

Robert Hromas, Rinah Shopnick, Hani George Jumean, Charles Bowers, Marileila Varella-Garcia, Kathleen Richkind

Research output: Contribution to journalArticlepeer-review

53 Scopus citations

Abstract

AML1 is a transcriptional activator that is essential for normal hematopoietic development. It is the most frequent target for translocations in acute leukemia. We recently identified 3 patients in whom pancytopenia developed almost 50 years after high-level radiation exposure from nuclear explosions during or after World War II. In all 3 patients, acute myeloid leukemia (AML) eventually developed that had similar characteristics and clinical courses. Cytogenetics from the 3 patients revealed a t(1;21)(p36;q22), a t(18;21)(q21; q22), and at(19;21)(q13.4;q22). By fluorescent in situ hybridization (FISH), all 3 translocations disrupted the AML1 gene. Two of these AML1 translocations, the t(18;21) and the t(19;21), have not been reported previously. It is possible that the AML1 gene is a target for radiation-induced AML. (C) 2000 by The American Society of Hematology.

Original languageEnglish (US)
Pages (from-to)4011-4013
Number of pages3
JournalBlood
Volume95
Issue number12
DOIs
StatePublished - Jun 15 2000
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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