Importance of the receptor and signal transduction of the granulocyte colony stimulating factor (G-CSF) in carcinoma of the ovary.

Rapid development of resistance in initially chemosensitive ovarian carcinomas is observed in 80% of all patients. One consequence of chemotherapy is myelosuppression, which can be avoided by applying granulocyte-colony stimulating factor (C-CSF). This prompts the question whether G-CSF could play a role in resistance development. A precondition for this is the presence of G-CSF-receptor on these tumour cells. Epithelial tumours like ovarian cancer, express considerably different forms of G-CSF-receptor. Clinically, this is of relevance for tumour initiation and progression. Concluding the results so far, rh (recombinant human) G-CSF could be a growth factor for some ovarian cancer cells. The different efficiency of G-CSF-receptor is possibly caused by the condition of the receptor: While wild-type (wt) G-CSF-receptor could lead to proliferation after ligation with its ligand, signal transduction by G-CSF receptor with a variant C-terminus is presumably not possible. Probably only 30% of all ovarian cancers have a wt-G-CSF receptor, 30% express a variant form and the rest are G-CSF-receptor negative. The expression of wt-G-CSF receptor is not obligatory for functional signal transduction.