Linked Life Data

11503967

Source:http://linkedlifedata.com/resource/pubmed/id/11503967

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-8-15
pubmed:abstractText
Human T-cell leukemia virus type I (HTLV-I) is the causative agent of adult T-cell leukemia/lymphoma (ATLL) and immortalizes human T cells interleukin-2 (IL-2)-dependently in vitro. Protracted culture of HTLV-I-infected T cells enables them to grow IL-2-independently. Although acquisition of IL-2-independent growth has been correlated with activation of signal transducers and activators of transcription (STATs), the precise mechanism of IL-2-independent growth is unknown. We found that expression of the Gfi-1 (growth factor independence-1) gene was elevated in most HTLV-I-transformed IL-2-independent cell lines but in few HTLV-I-infected IL-2-dependent cell lines. We also found elevated expression of Gfi-1 in fresh leukemic cells of ATLL patients. Although expression of Gfi-1 is correlated with activation of STAT3, induction of the dominant negative form of STAT3 in the HUT102 cell line does not alter the level of Gfi-1 expression. Furthermore, MT2 cells treated with Gfi-1 antisense oligonucleotide had reduced [3H]thymidine uptake compared with MT2 cells treated with Gfi-1 sense oligonucleotide. These findings indicate that Gfi-1 activation is involved in the IL-2-independent growth of HTLV-I-transformed T cells in vitro and in the development of ATLL in vivo, but is not induced by STAT activation.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0925-5710
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
507-16
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Expression of the Gfi-1 gene in HTLV-1-transformed T cells.
pubmed:affiliation
First Department of Internal Medicine, Ehime University School of Medicine, Shigenobu, Japan. ikusakai@m.ehime-u.ac.jp
pubmed:publicationType
Journal Article