Forced expression of AML1-AMP19, a fusion transcript generated from a radiation-associated t(19;21) leukemia, blocks myeloid differentiation

Heather Ramsey, Kent Christopherson, Robert Hromas

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

We isolated and characterized a novel AML1 (also termed Runx1) fusion transcript from a radiation-associated acute myeloid leukemia with a t(19;21). This fusion transcript, termed AML1-AMPl9, was joined out of frame, resulting in a truncated AML1 protein that inhibits activation of AML1 target promoters. It is now becoming clear that truncations of AMLl are more common in leukemia than previously thought. To analyze the effect of truncated AML1 species on myeloid differentiation and proliferation, AML1-AMPl9 was retrovirally transduced into the IL-3-dependent 32D cells. 32D cells over-expressing AML1-AMPl9 failed to differentiate normally when stimulated with G-CSF, but continued to proliferate and maintained a primitive phenotype. However, AML1-AMPl9 did not transform the cells to cytokine independence, implying that for full transformation of a myeloid progenitor by truncated AML1 another genetic lesion is required.

Original languageEnglish (US)
Pages (from-to)863-868
Number of pages6
JournalLeukemia Research
Volume28
Issue number8
DOIs
StatePublished - Aug 1 2004
Externally publishedYes

Keywords

  • AML
  • Leukemia
  • Myeloid differentiation

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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