Repair of the normal ovarian epithelium, subsequent to the damage inflicted by ovulation, is thought to be carried out by epidermal growth factor (EGF) acting through its receptor (EGFR). In many tumour cells, it has been shown  that the role of EGF is taken by transforming growth factor-α, (TGF-α,). In breast cancer, there is firm evidence that overexpression of EGFR is associated with poor prognosis , implying a role for this receptor in promoting tumour progression. Thus, TGF-α, may, through the EGF receptor, be a driving force in the growth of some ovarian cancers. If so, blocking either growth factor or receptor function may have therapeutic implications. This study set out to establish the levels and frequency at which TGF-α, and EGFR can be detected in human ovarian epithelial cancers. Concurrently, in an effort to create model systems for testing potential drugs, ovarian cancer cell lines and xenografts were established and characterized in terms of sensitivity to EGF/TGF-α, and the corresponding levels and frequency of detection of endogenous EGFR and TGF-α, determined.
KeywordsOvarian Cancer Epidermal Growth Factor Receptor Tyrosine Kinase Activity Human Ovarian Cancer Scatchard Analysis
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