The ovarian stroma after the menopause: activity and ageing

Loubet, R; Loubet, A; Leboutet, M.-J.

doi:10.1007/978-94-015-1129-2_9

Cited by 5 publications

(6 citation statements)

References 51 publications

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“…The demonstration of absence of aromatase in hormone-sensitive tumour is not without precedent since the enzyme has been reported to be absent from prostatic carcinomas known to have increased intra-tumoural oestrogen production and to be affected by oestrogen.P Peripheral aromatization increases with age in men and women. Loubet et al 30 in their review of ovarian stroma after the menopause hypothesized that cessation of follicular development and persistence of functional stroma might be correlated with changes in the vascular component, which preserved blood flow preferentially to the stroma. Stroma of postmenopausal ovaries are not quiescent, and most reports have agreed that androgen, not oestrogen, was the secretory product.…”

Section: Discussionmentioning

confidence: 99%

Lack of Evidence for Aromatase Expression in Human Ovarian Epithelial Carcinoma

et al. 1994

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SUMMARY. It is controversial whether ovarian epithelial carcinoma possesses steroidogenic enzymes. We investigated aromatase expression in ovarian epithelial carcinoma, and compared it with the normal ovary and placenta. Samples were obtained from an ovarian carcinoma cell line SK-OV-3, ovarian tumour tissues from four patients with epithelial carcinoma and one patient with dysgerminoma. Aromatase enzymatic activity was measured in microsome fractions by quantitating 3H 2 0 released from [1-3H] androstenedione and [3H] oestrone converted from [1,2,6,7-3H] androstenedione. Aromatase messenger ribonucleic acid (mRNA) was determined by reverse transcription-polymerase chain reaction (RT-PCR) using oligonucleotide primers synthesized according to the published human aromatase gene sequence.No aromatase activity was detected in either of two mucinous cystadenocarcinoma specimens or in SK-OV-3 cells, while aromatization proceeded with apparent MichaelisMenten kinetics in the normal ovaries and placentas. The apparent Km value was 200 nmollL for the ovary. Aromatase mRNA was detected in dysgerminoma, and the normal ovary and placenta, but not in any of three mucinous cystadenocarcinoma specimens, one serous cystadenocarcinoma specimen and SK-OV-3 cells. These results for both enzyme activity and gene expression suggest that the human ovarian epithelial carcinoma lacks aromatase. The demonstration of absence of aromatase gene expression raises the possibility that aromatase activity in ovaries bearing epithelial carcinoma may be associated with hyperplastic stromal rather than tumour cells.

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Section: Discussionmentioning

confidence: 99%

Lack of Evidence for Aromatase Expression in Human Ovarian Epithelial Carcinoma

et al. 1994

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“…1985) which in turn reduces unbound sex steroid levels. Sex steroids may play a role in the aetiology of stromal proliferation either as a direct mitogen, as suggested by Craig (1967), or via an effect on the vasculature of the ovarian stromal compartment (Loubet et al 1984). Alternatively, the primary association may be between infertility and stromal hyperplasia in later life particularly since the negative correlation between parameters and pregnancy is strongest when abortions (and hence most conceptions) are included in the analysis.…”

Section: Discussionmentioning

confidence: 99%

“…It may be associated with non-ovarian pathology, including endometrial carcinoma (Smith, Johnson & Hertig 1942, Woll et af. 1948, Novak & Mohler 1953, Schneidei-& Bechtel 1956, Sommers & lMeissner 1957, lMarcus 1963, Steams, Sneeden & Fear1 1974, Loubet, Loubet & Leboutet 1984, endometrial hyperplasia, endometrial polyps, uterine leiomyomas (Yin & Sommers 1961) and carcinoma of the breast (Sommers 8c Teloh 1952, McManus & Sommers 1952. In a study of 100 autopsies, Boss et al (1965) demonstrated an association between stromal hyperplasia and virilism, diabetes and hypertensive change.…”

Section: Introductionmentioning

confidence: 99%

“…Other workers have used a cortical thickness of greater than 2 mm as their criterion (Bigelow 1958, Craig 1967, Stearns et af. 1974, Loubet et al 1984 or have defined hyperplasia qualitatively, assessing, for example, the degree of nodularity, the size and shape ofcells and their nuclei and the collagen content of the stroma (Woll et al 1948, Sommers & Teloh 1952, Novak & Mohler 1953, Roddick & Greene 1957, 1958, Marcus 1963, Boss et al 1965, Rome et af. 1977, Lucisano et af.…”

Section: Introductionmentioning

confidence: 99%

“…Comparison of studies is hindered further by some workers using operative specimens (Roddick & Greene 1957, Marcus 1963, Craig 1967, Rome et al 1977, Loubet et a/. 1984, Lucisano et af.…”

Section: Introductionmentioning

confidence: 99%

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Morphometric assessment of ovarian stromal proliferation–a clinicopathological study

et al. 1989

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Ovarian stromal hyperplasia is commonly observed in peri- and post-menopausal ovaries. Assessment has, hitherto, been largely subjective or dependent on arbitrary criteria, which has made comparison of studies difficult. In this study, the stroma of a large number of ovaries was assessed morphometrically. Data were related to clinicopathological and cytomorphological information. A significant association was noted between the degree of stromal proliferation and post-menopausal endometrial adenocarcinoma (P = 0.004). There were no significant correlations between the degree of stromal proliferation and average cytomorphological dimensions.

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Effect of pituitary gonadotrophins on proliferation of primary cultures of human ovarian stroma

Snowden

Bradbury

Thornton

et al. 1989

The Journal of Pathology

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Proliferation of ovarian stromal cells is a common phenomenon in peri- and post-menopausal ovaries. It is generally assumed to be secondary to the rise in circulating gonadotrophins at the menopause, though the process by which it occurs is poorly understood. This study aimed to examine the effect of menopausal levels of pituitary gonadotrophins on the growth of primary cultures of ovarian stroma. A culture system was developed using primary explants of ovarian stroma on a collagen substrate. The effect of follicle stimulating hormone (FSH; 10(-5) g/l) and luteinizing hormone (LH; 10(-5) g/l) on the proliferation of cultures derived from the cortices and medullae of ten ovaries was evaluated using a dual radiothymidine labelling technique. FSH was stimulatory to cortical cultures from 9/10 ovaries and medullary cultures from 7/10 ovaries, while LH was stimulatory to cortical cultures from 6/9 ovaries and medullary cultures from 5/10 ovaries. The responsiveness of the cultures did not correlate with the degree of hyperplasia in vivo. This study demonstrates that pituitary gonadotrophins may modulate the growth of stromal cells in culture, and thus may play a role in the process whereby stromal proliferation occurs in peri- and post-menopausal ovaries.

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The ovarian stroma after the menopause: activity and ageing

Cited by 5 publications

References 51 publications

Lack of Evidence for Aromatase Expression in Human Ovarian Epithelial Carcinoma

Lack of Evidence for Aromatase Expression in Human Ovarian Epithelial Carcinoma

Morphometric assessment of ovarian stromal proliferation–a clinicopathological study

Effect of pituitary gonadotrophins on proliferation of primary cultures of human ovarian stroma

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