Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Thecoma”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMedDate not supplied

Malignant theca cell tumor of rat.

A large-sized ovarian tumor of theca cell origin was found in a female rat. The mass was located in the right ovary position. Histologically, the tumor was covered by thin fibrous capsule and consisted of a solid area and an abundant necrotic area. Tumor cells were arranged in a storiform or whorled pattern. Connective tissue elements occasionally presented as bundles of dense collagen fibers. Fusiform to elongated cells had oval- to spindle-shaped nuclei with indistinct nucleoli. Large round nuclei and mitotic figures were scattered throughout the tumor cells. These cells were stained positively with S-100 but negatively with vimentin and a-smooth muscle actin. Tumor cells with abundant cytoplasm sometimes contained multiple small-sized lipid vacuoles.

Animals↗
PubMed1992

Numerical chromosome aberrations in fibrothecoma.

Cytogenetic analysis on a 7-day-old culture of a fibrothecoma showed only numerical chromosome abnormalities: 57, XX, +4, +5, +6, +10, +12, +12, +14, +17, +18, +19, +20. The finding of an extra copy of chromosome 12 in mesenchymal tumors, mostly benign and originating from the female genital tract, may possibly point towards their common embryonic origin.

Adult↗
PubMed1977

Ovarian tumors and related lesions in aged chimpanzees.

The ovaries of a 48-year-old chimpanzee each contained a large bilateral fibrothecoma. A 39-year-old chimpanzee had two small fibrothecomas in one ovary and a well-differentiated Sertoli-Leydig cell tumor in the other; there also was adenomatous hyperplasia of the endometrium. Both animals had extensive thecal hypertrophy in the ovaries. Thecal hypertrophy might have been a source of excessive estrogen and could have been a partial cause of the ovarian tumors.

Animals↗
PubMed2003

Malignant granulosa-theca cell tumor in a two-year-old Miniature Horse.

A 2-year-old female Miniature Horse that presented with a history of progressive weight loss, depression, and diarrhea was diagnosed at necropsy with a highly malignant abdominal neoplasm involving the left ovary, kidneys, adrenal glands, intestines, and various abdominal and thoracic lymph nodes. Microscopic examination of these masses revealed large pleomorphic cells that stained positive for vimentin and inhibin and negative for epithelial membrane antigen and placental alkaline phosphatase. Ultrastructural examination of the cells revealed a high nucleocytoplasmic ratio and indented euchromatic nuclei with large nucleoli. Based on the gross, microscopic, immunohistochemical, and ultrastructural features, the neoplasm was identified as a malignant granulosa-theca cell tumor, a rare neoplasm in young horses.

Animals↗
PubMed2002

Prevention of thecal angiogenesis, antral follicular growth, and ovulation in the primate by treatment with vascular endothelial growth factor Trap R1R2.

This study was designed to investigate the effects of inhibition of thecal angiogenesis on follicular development in the marmoset monkey (Callithrix jacchus). To inhibit vascular endothelial growth factor (VEGF), a soluble combined truncated form of the fms-like tyrosine kinase (Flt) and kinase insert domain-containing receptor (KDR) receptor fused to IgG (VEGF Trap R1R2) was administered for 10 d during the follicular phase of the cycle. Changes in angiogenesis and follicular cell proliferation were quantified using immunocytochemistry for bromodeoxyuridine to obtain a proliferation index, CD31 to visualize endothelial cell area, and dual staining to distinguish thecal endothelial cell proliferation. The effects of the treatment on follicular development were assessed by morphometric analyses by measuring follicle diameter, thecal thickness, and a proliferation index for granulosa cells. Follicular atresia was detected and quantified using the terminal deoxynucleotidyltransferase-UTP nick end labeling method. Effects on gene expression of VEGF and its receptors, Flt and KDR, were studied by in situ hybridization. VEGF Trap R1R2 treatment resulted in a significant decrease in thecal proliferation and endothelial cell area, demonstrating the suppression of thecal angiogenesis. The absence of a normal thecal vasculature was associated with a significantly reduced thecal thickness. Antral follicular development was severely compromised, as indicated by decreased granulosa cell proliferation, decreased follicular diameter, and lack of development of ovulatory follicles. Furthermore, the rate of atresia was significantly increased. VEGF expression in granulosa and thecal cells increased after treatment, whereas Flt and KDR expressions in thecal endothelial cells were markedly decreased. These results show that VEGF Trap treatment is associated with the suppression of follicular angiogenesis, which results in the inhibition of antral follicular development and ovulation.

Angiogenesis Inhibitors↗
PubMed1978

Postmenopausal virilization due to ovarian stromal hyperthecosis.

A 53-year-old woman presented with hirsutism of long duration and virilization of recent onset. She was gravida 12 para 9. The 17-ketosteroids were normal, gonadotropins were in the post-menopausal range, and the serum testosterone was in the male range. After bilateral oophorectomy, the testosterone became normal. Ovarian pathology revealed stromal hyperthecosis.

17-Ketosteroids↗
PubMed2000

Bone morphogenetic protein inhibits ovarian androgen production.

Bone morphogenetic proteins (BMPs), members of the transforming growth factor beta superfamily, were recently shown to be expressed and to regulate steroidogenesis in rat ovarian tissue. The purpose of this study was to investigate the effect of BMP-4 on androgen production in a human ovarian theca-like tumor (HOTT) cell culture model. We have previously demonstrated the usefulness of these cells as a model for human thecal cells. HOTT cells respond to protein kinase A agonists by increased production of androstenedione and with an induction of steroid-metabolizing enzymes. In this investigation, HOTT cells were treated with forskolin or dibutyryl cyclic AMP (dbcAMP) in the presence or absence of various concentrations of BMP-4. The accumulation of androstenedione, progesterone, and 17alpha-hydroxyprogesterone (17OHP) in the incubation medium was measured by RIA. The expression of 17alpha-hydroxylase (CYP17), 3beta-hydroxysteroid dehydrogenase (3betaHSD), cholesterol side-chain cleavage (CYP11A1), and steroidogenic acute regulatory (StAR) protein was determined by protein immunoblotting analysis using specific rabbit polyclonal antibodies. We also examined the expression of BMP receptor subtypes in our HOTT cells using RT-PCR. In cells treated with medium alone, steroid accumulation and steroid enzyme expression was unchanged. In cells treated with BMP alone there was a modest decrease in androstenedione secretion. In the presence of forskolin, HOTT cell production of androstenedione, 17OHP, and progesterone increased by approximately 4.5-, 35-, and 3-fold, respectively. In contrast, BMP-4 decreased forskolin-stimulated HOTT cell secretion of androstenedione and 17OHP by 50% but increased progesterone production 3-fold above forskolin treatment alone. Forskolin treatment led to an increase in CYP17, CYP11A1, 3betaHSD, and StAR protein expression. BMP-4 markedly inhibited forskolin stimulation of CYP17 expression but had little effect on 3betaHSD, CYP11A1, or StAR protein levels. Similar results were observed with the cAMP analog dbcAMP. In addition, BMP-4 inhibited basal and forskolin stimulation of CYP17 messenger RNA expression as determined by RNase protection assay. Other members of the transforming growth factor beta superfamily, including activin and inhibin, had minimal effect on androstenedione production in the absence of forskolin. In the presence of forskolin, activin inhibited androstenedione production by 80%. Activin also inhibited forskolin induction of CYP17 protein expression as determined by Western analysis. We identified the presence of messenger RNA for three BMP receptors (BMP-IA, BMP-IB, and BMP-II) in the HOTT cells model. In conclusion, BMP-4 inhibits HOTT cell expression of CYP17, leading to an alteration of steroidogenic pathway resulting in reduced androstenedione accumulation and increased progesterone production. These effects of BMP-4 seem similar to those caused by activin, another member of the transforming growth factor-beta superfamily of proteins.

Androgens↗
PubMed1998

Direct luteinizing hormone action triggers adrenocortical tumorigenesis in castrated mice transgenic for the murine inhibin alpha-subunit promoter/simian virus 40 T-antigen fusion gene.

Transgenic (TG) mice, expressing the Simian Virus 40 T-antigen (Tag) under a 6-kb fragment of the murine inhibin alpha-subunit promoter (inh alpha p), develop gonadal tumors of granulosa/theca or Leydig cell origin. We showed previously that adrenocortical tumors develop if the TG mice are gonadectomized but never develop in intact animals. However, if functional gonadectomy was induced by GnRH antagonist treatment or by cross-breeding the TG mice into the hypogonadotropic hpg genetic background, neither gonadal nor adrenal tumors appeared. Since the most obvious difference between the gonadectomized and GnRH-antagonist-treated or Tag/hpg double mutant mice is the elevated gonadotropin secretion in the first group, we examined whether the adrenal tumorigenesis would be gonadotropin-dependent. Surprisingly, both the adrenal tumors and a cell line (C alpha 1) derived from one of them expressed highly functional LH receptors (LHR), as assessed by Northern hybridization, immunocytochemistry, ligand binding, and human CG (hCG)-stimulated cAMP and steroid production. No FSH receptor expression was found in the adrenal tumors by RT-PCR. hCG treatment of the C alpha 1 cells stimulated their proliferation, as measured by [3H]thymidine incorporation. This effect was related to hCG-stimulated steroidogenesis since progesterone, testosterone, and estradiol, at physiological concentrations, also stimulated the C alpha 1 cell proliferation. Different adrenocortical cells expressed initially LHR and Tag, whereas both were highly expressed in the tumor cells. In conclusion, the high level of functional LHR in the adrenal tumors indicates that this receptor can function as tumor promoter when ectopically expressed and stimulated by the ligand hormone.

Adrenal Cortex Neoplasms↗