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Abnormal expression of FLI1 protein is an adverse prognostic factor in acute myeloid leukemia

Steven M Kornblau1, Yi Hua Qiu, Nianxiang Zhang

  • 1Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA. skornblau@mdanderson.org

Blood
|September 16, 2011
PubMed

Insights

Friend leukemia virus integration 1 (FLI1) expression is frequently abnormal in acute myelogenous leukemia (AML). High FLI1 levels are linked to shorter remission duration and survival, suggesting it as a potential therapeutic target.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Friend leukemia virus integration 1 (FLI1) is an Ets transcription factor implicated in acute myelogenous leukemia (AML) through chromosomal abnormalities.
  • The biological significance of FLI1 expression in AML pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the impact of FLI1 protein expression on the clinical course and outcomes of AML patients.
  • To explore the correlation of FLI1 expression with specific genetic mutations and protein interactions in AML.

Main Methods:

  • FLI1 protein expression was quantified in 511 newly diagnosed AML patients.
  • Expression levels were compared between diagnostic and relapse samples, peripheral blood, and bone marrow.
  • Correlations with patient characteristics, genetic mutations (NPM1, FLT3-ITD), and protein expression profiles were analyzed.

Main Results:

  • FLI1 expression was higher at diagnosis than relapse and varied significantly in AML patients compared to normal cells.
  • Elevated FLI1 levels were associated with mutated NPM1 or FLT3-ITD and negatively correlated with antecedent hematologic disorders.
  • Low or high FLI1 expression correlated with shorter remission duration and overall survival, with high FLI1 being an adverse prognostic factor.

Conclusions:

  • FLI1 expression is frequently abnormal in AML and carries a poor prognosis.
  • FLI1 and its downstream targets represent potential therapeutic targets for AML intervention.

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