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.