Differential levels of soluble endoglin (CD105) in myeloid malignancies

Luana Calabrò, Ester Fonsatti, Giacomo Bellomo, Andrea Alonci, Francesca Colizzi, Luca Sigalotti, Maresa Altomonte, Caterina Musolino, Michele Maio

Research output: Contribution to journalArticle

Abstract

Angiogenesis contributes to disease progression in solid and hematopoietic malignancies, and endoglin (CD105), a component of the transforming growth factor (TGF)-β receptor complex, is a powerful marker of neovascularization. Elevated amounts of soluble CD105 (sCD105) have been recently identified in selected solid tumors but no data are available on sCD105 in hematopoietic malignancies. Therefore, levels of sCD105 were investigated in sera of patients with acute myeloid leukemia (AML) (n = 10) or chronic myeloproliferative disorders (CMD) (n = 28), and correlated with those of soluble TGF-β1 (sTGF-β1). Dot blot assay detected higher amounts of sCD105 (P <0.05) both in AML (4.34 ± 2.62 OD/ mm2) and in CMD (3.71 ± 2.09 OD/mm2) patients than in healthy subjects (n = 14, 2.38 ± 1.18 OD/mm2). Instead, enzyme-linked immunosorbent assay (ELISA) identified (P <0.05) lower and higher levels of sTGF-β1 in AML (32,017 ± 1,900 pg/ ml) and CMD (60,700 ± 19,200 pg/ml) patients, respectively, compared to healthy individuals (n = 11, 47,173 ± 5,443 pg/ml). In essential thrombocythemia (ET) patients with thrombotic episodes, levels of sCD105 were lower (P <0.05) compared to patients without thrombotic complications, and inversely correlated with those of sTGF->1 (r = 0.94). Conversely, amounts of sCD105 directly correlated with levels of sTGF-β1 (r=0.74) in ET patients without thrombotic events. Our results show that high levels of sCD105 are present in myeloid malignancies that are characterized by a high cellular proliferation rate, and suggest that an altered balance between sCD105 and sTGF-β1 might favor disease progression and clinical complications.

Original languageEnglish
Pages (from-to)171-175
Number of pages5
JournalJournal of Cellular Physiology
Volume194
Issue number2
DOIs
Publication statusPublished - Feb 1 2003

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

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