Linked Life Data

12494455

Source:http://linkedlifedata.com/resource/pubmed/id/12494455

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-12-20
pubmed:abstractText
Angiogenesis contributes to disease progression in solid and hematopoietic malignancies, and endoglin (CD105), a component of the transforming growth factor (TGF)-beta 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-beta(1) (sTGF-beta(1)). Dot blot assay detected higher amounts of sCD105 (P < 0.05) both in AML (4.34 +/- 2.62 OD/mm(2)) and in CMD (3.71 +/- 2.09 OD/mm(2)) patients than in healthy subjects (n = 14, 2.38 +/- 1.18 OD/mm(2)). Instead, enzyme-linked immunosorbent assay (ELISA) identified (P < 0.05) lower and higher levels of sTGF-beta(1) 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-beta(1) (r = 0.94). Conversely, amounts of sCD105 directly correlated with levels of sTGF-beta(1) (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-beta(1) might favor disease progression and clinical complications.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9541
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
194
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
171-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12494455-Acute Disease, pubmed-meshheading:12494455-Adolescent, pubmed-meshheading:12494455-Adult, pubmed-meshheading:12494455-Aged, pubmed-meshheading:12494455-Aged, 80 and over, pubmed-meshheading:12494455-Antigens, CD, pubmed-meshheading:12494455-Chronic Disease, pubmed-meshheading:12494455-Female, pubmed-meshheading:12494455-Humans, pubmed-meshheading:12494455-Leukemia, Myeloid, pubmed-meshheading:12494455-Male, pubmed-meshheading:12494455-Middle Aged, pubmed-meshheading:12494455-Myeloproliferative Disorders, pubmed-meshheading:12494455-Receptors, Cell Surface, pubmed-meshheading:12494455-Solubility, pubmed-meshheading:12494455-Transforming Growth Factor beta, pubmed-meshheading:12494455-Transforming Growth Factor beta1, pubmed-meshheading:12494455-Vascular Cell Adhesion Molecule-1
pubmed:year
2003
pubmed:articleTitle
Differential levels of soluble endoglin (CD105) in myeloid malignancies.
pubmed:affiliation
Cancer Bioimmunotherapy Unit, Department of Medical Oncology, Centro di Riferimento Oncologico, I.R.C.C.S., Aviano, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't