Expression of angiopoietins and their receptor Tie2 in the bone marrow of patients with acute myeloid leukemia

Haematologica. 2006 Sep;91(9):1203-11.

Abstract

Background and objectives: Angiopoietin-1 (Ang-1) and its natural antagonist angiopoietin-2 (Ang-2), both ligands for the receptor tyrosine kinase Tie2, are known to play an essential role in normal and pathological angiogenesis.

Design and methods: We investigated the expression of Ang-1, Ang-2 and Tie2 by immunohistochemical analyses in bone marrow biopsies of 64 adult patients with newly diagnosed acute myeloid leukemia (AML) and correlated angiogenic factor expression with clinicopathological variables and long-term survival.

Results: Expression of Ang-2 was significantly higher in the bone marrow of AML patients than in 16 control patients. In contrast, the levels of Ang-1 expression in AML patients did not differ from those found in controls. Thus, we observed a reversal of the Ang-1 and Ang-2 expression balance in the neoplastic bone marrow. Furthermore, Tie2 was significantly overexpressed in leukemic blasts. Patients expressing high levels of Ang-2 had significantly longer overall survival than those with low Ang-2 levels (52.7 vs. 14.7 months). Multivariate analysis revealed that karyotype and Ang-2 expression were independent prognostic factors for overall survival (hazard ratio [CI]: 3.06 [1.39-6.70] and 0.31 [0.14-0.69], respectively).

Interpretation and conclusions: These data provide evidence that the alteration of angiopoietin balance in favor of Ang-2 may play a critical role in the pathophysiology of AML. Furthermore, high pre-therapeutic levels of Ang-2 in the bone marrow indicate a favorable prognosis in AML patients treated with polychemotherapy, although the mechanism is not yet known.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Angiopoietin-1 / genetics
  • Angiopoietin-2 / genetics
  • Angiopoietins / genetics*
  • Bone Marrow / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Leukemia, Myeloid / genetics*
  • Receptor, TIE-2 / genetics*

Substances

  • Angiopoietin-1
  • Angiopoietin-2
  • Angiopoietins
  • Receptor, TIE-2