| pubmed-article:9681250 | 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. | lld:pubmed |
