Linked Life Data

10374864

Source:http://linkedlifedata.com/resource/pubmed/id/10374864

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1999-7-7
pubmed:abstractText
Bone marrow (BM) cells that were concentrated for hematopoietic progenitor cells by in vivo treatment with 5-FU were infected with a recombinant retrovirus containing a human full-sized, non-spliced type WT1 (Wilms' tumor gene 1) cDNA and then colony-assayed in the presence of granulocyte-colony stimulating factor (G-CSF). Significantly more colony-forming units granulocyte-monocyte (CFU-GM), colony-forming units granulocyte (CFU-G), and colony-forming units monocyte (CFU-M) colonies were formed in response to G-CSF from the BM cells infected with the WT1-containing retrovirus than from the control BM cells infected with an empty vector. Furthermore, FACS analysis of cell surface differentiation markers showed the inhibition of differentiation by constitutive WT1 expression resulting from the infection with the WT1-containing retrovirus. These results thus showed that the constitutive WT1 expression promoted the proliferation of myeloid progenitor cells but inhibited their differentiation in response to G-CSF, suggesting the alteration of G-CSF signaling pathway. The results also supported our hypothesis that the WT1 gene performs an oncogenic rather than a tumor suppressor gene function in hematopoietic progenitor cells, although the WT1 gene potentially performs both functions. This finding implies an important role of the WT1 gene in leukemogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0145-2126
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
499-505
pubmed:dateRevised
2006-4-21
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Constitutive expression of the Wilms' tumor gene WT1 inhibits the differentiation of myeloid progenitor cells but promotes their proliferation in response to granulocyte-colony stimulating factor (G-CSF).
pubmed:affiliation
Department of Medicine III, Osaka University Medical School, Suita City, Japan.
pubmed:publicationType
Journal Article