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• W2490671640 abstract "Ovarian cancer arises almost exclusively in epithelial cells derived from the surface of the ovary. It is thought that the continual damage caused by ovulation (break of the epithelial surface layer to allow release of the follicle) and the subsequent repairs are the prime factors in promoting ovarian epithelial cancer. The prime promoter of growth repair is epidermal growth factor (EGF). EGF works through the EGF receptor (EGFr) and EGFr has been detected in about 45% of ovarian cancer. Epidermal growth factor and transforming growth factor alpha are two peptides which bind to the epidermal growth factor receptor. Although the literature shows that epidermal growth factor (EGF) was detected in less than 30% of ovarian cancers, transforming growth factor alpha (TGFalpha) was present in 88.5%. To investigate the possible role of growth factors in ovarian carcinoma, the OAW42 epithelial ovarian cancer cell line (previously established from ascites of patient with ovarian cancer) was used as a model. To allow these studies to be extended to the effects of drug resistance, PEO1 and PEO1cddp cells were used (PEO1 was a platinum sensitive cell line, PEO1cddp a platinum resistant cell line). Growth stimulation of OAW42 cells over 48 and 72 hours by TGFalpha reached a maximum of 42 and 19.6% above control respectively at 10 ng/ml dose. Growth stimulation by TGFalpha was seen in PEO1 cells as early as 24 hours, reaching a maximum of 35% above control at 25 ng/ml. Growth response to EGF showed that OAW42 cells responded positively to the influence of EGF after 48 and 72 hours reaching a maximum of 34% above control at 10 ng/ml. PEO1 cells again showed earlier stimulation of growth by EGF reaching a maximum of 18.9% after 24 hours, 30.8% at 48 hours, and 16.1% after 72 hours at dose of EGF (2.5 ng/ml). Both cell lines were, EGFr positive, as expected. After 24 hours exposure of PEO1cddp cells to EGF, a slight stimulation of growth was seen at a dose of 5 ng/ml (about 6.3% above control). After 48 hours no stimulation of cell proliferation seen. At 72 hours exposure PEO1cddp cell growth was inhibited by all concentrations of EGF, suggesting that acquision of drug resistance was also associated with changed response to EGF. TGFalpha, a known inhibitor of the proliferation of normal ovarian epithelial cells was shown to inhibit growth of OAW42 cells over 96 hours reaching a maximum of 35% at 5 ng/ml. After treating OAW42 cells with luteinzing hormone (LH), cells showed inhibition of growth reaching a maximum of 21, 26.2, and 30.1% after 24, 48, and 72 hours respectively at 60 iu/1 dose of LH. PEO1 cells showed growth inhibition, reaching a maximum of 34.2, 26.9, and 32.8% below control after 24, 48, and 72 hours respectively at 60 iu/l dose of LH. Anti-TGFalpha polyclonal antibody (5 ?l/ml) reversed LH-induced inhibition of growth. A further increase of anti-TGFalpha antibody up to 30 ?l/ml gave growth stimulation of 11.3% above control cells suggesting that TGFalpha is normally having some inhibitory effects on the cells under control conditions in addition to mediating the LH response. Cancer and other hyperproliferative diseases often show elevated protein tyrosine kinase (PTK) activity, related to the increased activity of growth factor receptors. In the present study, there was growth inhibition of OAW42 cells over 72 hours by blocking PTK with an EGF receptor specific tyrosine kinase inhibitor, reaching a maximum of 38.3% below control cell growth at 3.0 muM dose. PEO1 and PEO1cddp cells were also growth inhibited by increasing concentrations of TKI from (0.5 to 3.0 muM) reaching a maximum of 55.0 and 59.3% below control respectively at 3.0 muM dose. This confirmed the importance of EGF as a growth promoter in at least some ovarian cancers. Electron microscopy was used to study the hormonaly-induced changes in the cellular morphology of ovarian cancer cells. The actions of LH were compared with those of epidermal growth factor (EGF). Exposure of OAW42 cells to EGF at 10 ng/ml dose for up to 72 hours showed swollen mitochondria, more evidence of polysomes and more stubby microvilli, in keeping with the growth response to EGF seen after 72 hours incubation. The effect of LH showed no evidence of swollen mitochondria, no prominent polysomes and few stubby microvilli, this time reflecting the growth inhibition of higher doses of LH. On the basis of the results described in this thesis, new therapies for ovarian cancer may be based on either regulation of the EGF receptor or promotion of the action of TGFalpha." @default.
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• W2490671640 date "1997-01-01" @default.
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• W2490671640 title "Growth regulation of ovarian cancer" @default.
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