Linked Life Data

9681250

Source:http://linkedlifedata.com/resource/pubmed/id/9681250

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-10-8
pubmed:abstractText
A variety of non-hematopoietic malignant tumors have been demonstrated to secrete granulocyte colony-stimulating factor (G-CSF) in amounts large enough to cause a significant systemic hematopoietic effect. Meanwhile, bladder cancer cells have been shown to secrete a variety of biological factors with no direct relation to urothelial cell origin. G-CSF produced by non-hematopoietic malignant cells in particular has been reported to be capable of inducing a leukemoid reaction in the host through intense stimulation of leukocyte production. This is most frequently associated with aggressive tumor cell growth and a poor clinical outcome. On the other hand, receptors for G-CSF have also been found on the cell surfaces of several non-hematopoietic cell types. These observations lead naturally to the tempting speculation that simultaneous acquisition of the ligand promotion and its receptor expression by a malignant tumor may provide a strong autocrine growth advantage. However, the role of autocrine growth factors in malignancy is even less clear, although it is undoubtedly important. In this review, G-CSF and tumor cell growth, particularly of human transitional cell carcinomas of the bladder, are discussed, and autocrine growth of human solid tumors is also summarized.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1368-4736
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
G-CSF production in human bladder cancer and its ability to promote autocrine growth: a review.
pubmed:affiliation
Department of Urology, School of Medicine, Keio University, Japan.
pubmed:publicationType
Journal Article, Review