Growth Regulation of Ovarian Cancer

Godwin, Andrew K.; Perez, Raymond P.; Johnson, Steven W.; Hamaguchi, K; Hamilton, Thomas C.

doi:10.1016/s0889-8588(18)30312-5

Cited by 31 publications

(20 citation statements)

References 63 publications

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“…It was suggested that inclusion cysts in ovarian cortex lie in proximity to steroid hormone-producing cells in the vasculature and are exposed to paracrine ovarian androgens (36,37). Consistently, high androgen level is a significant risk factor in ovarian cancer (36,38), indicating the involvement of theca cell activity.…”

Section: Gt198 Mutations In Ovarian Cancer Stromamentioning

confidence: 99%

Human Ovarian Cancer Stroma Contains Luteinized Theca Cells Harboring Tumor Suppressor Gene GT198 Mutations

Peng¹,

Zhang

Jaafar

et al. 2013

Journal of Biological Chemistry

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Background: GT198 is a tumor suppressor gene in breast and ovarian cancer. Results: Tumor stromal cells in various types of human ovarian cancer carry GT198 mutations and express theca cell-specific enzyme CYP17. Conclusion: GT198 mutant tumor stromal cells are luteinized theca cells in ovarian cancer. Significance: Studying mutant tumor stromal cells is crucial for understanding the cause of ovarian cancer.

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Section: Gt198 Mutations In Ovarian Cancer Stromamentioning

confidence: 99%

Human Ovarian Cancer Stroma Contains Luteinized Theca Cells Harboring Tumor Suppressor Gene GT198 Mutations

Peng¹,

Zhang

Jaafar

et al. 2013

Journal of Biological Chemistry

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“…The gonadotropin hypothesis suggests that an excessive production of gonadotropins (such as luteinizing hormone) can stimulate proliferation and malignant transformations of ovarian epithelium either directly (7) or indirectly through increased ovarian production of androgens (2). Suggestions for an involvement of androgens in ovarian cancer come from in vitro studies and animal experiments (8)(9)(10)(11), in which androgens were found to stimulate ovarian epithelial cell proliferations. This hypothesis is also corroborated by the association of polycystic ovary syndrome (a syndrome associated with increased ovarian androgen secretion) with an increased risk of ovarian cancer (3) and the protective effect of oral contraceptives, which suppress androgen synthesis.…”

Section: Introductionmentioning

confidence: 99%

Endogenous Androgens and Risk of Epithelial Ovarian Cancer: Results from the European Prospective Investigation into Cancer and Nutrition (EPIC)

Rinaldi¹,

Dossus

Lukanova

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Few epidemiologic studies have examined the hypothesis that circulating androgens are involved in the development of ovarian cancer. We investigated the association between prediagnostic serum levels of androgens and sex hormonebinding globulin (SHBG) and ovarian cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort. One hundred and ninety-two ovarian cancer cases and 346 matched controls not using exogenous hormones at baseline blood donation were eligible for the study. Serum levels of testosterone, androstenedione, dehydroepiandrosterone sulfate, and SHBG were measured by direct immunoassays. Free testosterone (fT) was calculated according to mass action laws. Multivariate conditional logistic regression was used to estimate odds ratios adjusted for possible confounders. Overall, there was no association between serum concentrations of androgens or SHBG and ovarian cancer risk. In postmenopausal women, fT concentrations were inversely related to risk [highest versus lowest tertile odds ratio 0.45 (0.24-0.86); P trend = 0.01]. Among women diagnosed before the age of 55 years, there was a negative association with SHBG and a positive association with fT and ovarian cancer risk, although these associations were not statistically significant. The present study suggests that circulating androgens and SHBG levels are not strongly associated with ovarian cancer risk, although levels of fT may be associated with an increased risk among women diagnosed at relatively young age. The heterogeneity of results on the associations of fT with ovarian cancer risk in postmenopausal women deserves further investigation. (Cancer Epidemiol Biomarkers Prev 2007;16(1):23 -9)

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“…Gonadotropins stimulate growth of normal rabbit OSE cells . Both rat (Godwin et al, 1992) and human (Rodriquez et al, 1991) OSE cells proliferate in response to EGF and TGF-a, and EGF receptors have been identi®ed in human OSE cells (Jindal et al, 1994;Berchuck et al, 1991). Although TGF-b receptors have yet to be found on human OSE cells, TGF-b has been shown to inhibit the proliferation of these cells in culture (Berchuck et al, 1992) implying the presence of the receptor for this growth factor.…”

Section: Introductionmentioning

confidence: 99%

Transforming growth factor-β regulates Kit ligand expression in rat ovarian surface epithelial cells

1999

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In preparation for ovulation, paracrine communication between the preovulatory follicle and overlying theca/ stromal cells and ovarian surface epithelium (OSE) must take place to facilitate the degradative and apoptotic events associated with ovulation. Kit tyrosine kinase receptors and their ligand, kit ligand (KL) are expressed within ovarian follicles, and ligand-induced receptor activation appears to account for some of the cell ± cell interactions important for oocyte development. We investigated the expression of Kit receptors and KL in OSE cells and the possibility that modulation of their expression could a ect OSE cell activity. KL mRNA and protein were detected in the OSE cell layer of rat ovaries, and primary cultures of rat OSE as well as the immortalized rat OSE cell line, ROSE 199, expressed KL, but not Kit receptors. Both primary and immortalized OSE cells preferentially expressed KL-1, rather than KL-2, transcripts, suggesting that these cells produce predominantly the soluble form of KL. Activation of the cAMP signalling pathway using dibutyryl cAMP decreased proliferation of ROSE 199 cells and elicited a threefold increase in KL expression. TGF-b similarly inhibited ROSE 199 cell proliferation, but strongly inhibited dibutyryl cAMP-induced KL expression, indicating that changes in KL expression were not directly associated with OSE cell proliferation. The expression of mostly soluble KL in the surface epithelium suggests that this cytokine may be acting in a paracrine fashion, perhaps interacting with nearby Kit receptorbearing theca cells.

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Growth Regulation of Ovarian Cancer

Cited by 31 publications

References 63 publications

Human Ovarian Cancer Stroma Contains Luteinized Theca Cells Harboring Tumor Suppressor Gene GT198 Mutations

Human Ovarian Cancer Stroma Contains Luteinized Theca Cells Harboring Tumor Suppressor Gene GT198 Mutations

Endogenous Androgens and Risk of Epithelial Ovarian Cancer: Results from the European Prospective Investigation into Cancer and Nutrition (EPIC)

Transforming growth factor-β regulates Kit ligand expression in rat ovarian surface epithelial cells

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