Effect of a gonadotropin releasing hormone analog on an experimental ovarian tumor: Direct and indirect actions

Lux‐Lantos, Victoria; Thyssen, Sandra M.; Chamson, Astrid; Libertun, Carlos

doi:10.1016/0024-3205(95)00272-8

Cited by 18 publications

(13 citation statements)

References 32 publications

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“…In rats bearing intrasplenic ovarian autotransplants, peripheral steroid levels are not elevated, due to shunt of blood flow to the liver, where they are metabolized (3). However, active steroidogenesis is indicated by high StAR protein expression, in agreement with progesterone and estradiol secretion into the splenic vein, which collects tumor output (3). StAR was demonstrated only in luteinized follicles and in thecal cells, but was absent from granulosa cells of follicles, indicating that the latter do not participate in de novo steroid production, in agreement with previous data (24,46).…”

Section: Discussionsupporting

confidence: 80%

“…This tumor grows and acquires approximately three times the initial volume of the grafted estrous ovary after 2 months (3) and 20 times after 1 year of development (4). We have demonstrated that this tumor depends on gonadotropins for its growth by treating tumorbearing rats with buserelin, a gonadotropin-releasing hormone (GnRH) agonist that downregulates LH and FSH secretion; this resulted in very significant tumor regression (3). A direct action of GnRH analogs on the tumor has also been demonstrated (5,6).…”

Section: Introductionmentioning

confidence: 99%

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Development of an experimental ovarian tumor: immunocytochemical analysis

Sorianello

Fritz

Beyer

et al. 2002

European Journal of Endocrinology

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Objective: The aim of the present work was to study whether immunocytochemical parameters present in the normal ovary were altered after tumor development under high gonadotropin levels. Methods: Ovarian tumors (luteoma): castrated female rats had an ovary grafted into the spleen; tumors were left to develop for 1, 2, 3 or 7 months. The presence of apoptotic cells (TUNEL method) and the expression of proliferating cell nuclear antigen (PCNA), gap junction protein (Cx43), steroidogenic acute regulatory protein (StAR), aromatase and synaptosome-associated protein of 25 kDa (SNAP-25) were determined by immunocytochemistry. Some of these findings were confirmed by RT-PCR (Cx43, StAR, SNAP-25). Inhibin subunit mRNAs were investigated by Northern blot. Results: PCNA staining of tumors was mainly found in granulosa cells of transforming follicles and was absent from luteinized follicles. A nearly complete absence of apoptosis was observed. Cx43 was mainly found in follicles, while it was very weakly expressed or absent in luteinized follicles. StAR protein expression, indicating active steroidogenesis, was demonstrated only in luteinized follicles and in thecal cells, but was absent from granulosa cells. Aromatase immunoreactivity was very intense in granulosa and also present in luteal cells. Membrane-associated and cytoplasmic SNAP-25 immunostaining was determined in patches of endocrine cells in the follicles, as well as in the luteinized follicles. The expression of mRNAs for Cx43, StAR and SNAP-25 (RT-PCR) and inhibin subunits (Northern blots) were confirmed in 1-, 3-and 7-month-old tumors. Conclusions: These results indicated that luteoma most likely develop from unruptured follicles by hypertrophy and proliferation of follicular cells. Circulating gonadotropins seem to play a fundamental role in maintaining the expression of proteins typically expressed in normal ovary, while avoiding apoptosis in this tissue.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Development of an experimental ovarian tumor: immunocytochemical analysis

Sorianello

Fritz

Beyer

et al. 2002

European Journal of Endocrinology

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“…Tumor-bearing animals: rats were bilaterally ovariectomized and one ovary was implanted into the spleen, as previously described (Chamson-Reig et al, 1997;Lux et al, 1984;Lux-Lantos et al, 1995). Luteinized ovarian tumors (Luteoma) were left to develop for the required periods of time for each experimental design.…”

Section: Animalsmentioning

confidence: 99%

“…Cells from superovulated prepubertal ovaries were selected as a classical model for luteal cells and the intrasplenic ovarian tumor, histologically defined as a Luteoma, as a model of ovarian hyperplasic tissue of predominantly luteinized cells. This Luteoma is gonadotropin-dependent, endocrinally active and grows considerably during one year of development, not evidencing malignant transformation (Chamson-Reig et al, 1997;Chamson-Reig et al, 1999a;Hockl et al, 2003;Lux-Lantos et al, 1995). GnRH analog administration induced in vivo Luteoma regression (Chamson-Reig et al, 1997;Lux-Lantos et al, 1995).…”

mentioning

confidence: 95%

“…This Luteoma is gonadotropin-dependent, endocrinally active and grows considerably during one year of development, not evidencing malignant transformation (Chamson-Reig et al, 1997;Chamson-Reig et al, 1999a;Hockl et al, 2003;Lux-Lantos et al, 1995). GnRH analog administration induced in vivo Luteoma regression (Chamson-Reig et al, 1997;Lux-Lantos et al, 1995). In vitro stimulation of GnRH receptors present in the Luteoma induced signaling through a non-classical pathway, involving cAMP production, MAPK phosphorylation and total absence of phospholipase C activation (Chamson-Reig et al, 1999b;Chamson-Reig et al, 2003), in contrast to ovarian luteinized cells from superovulated prepubertal rats (SPO) in which the main GnRH signaling pathway was PLC activation.…”

mentioning

confidence: 97%

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