Growth-stimulatory effects of androgen, high concentration of glucocorticoid or fibroblast growth factors on a cloned cell line from Shionogi carcinoma 115 cells in a serum-free medium.

The effects of various kinds of growth factors or steroids on the proliferation of Shionogi carcinoma 115 (SC115) cells were investigated in cell culture. In a serum-free medium [Ham's F-12:Eagle's minimum essential medium (1:1, vol/vol) containing 0.1% bovine serum albumin], the proliferation of SC-3 cells (a cloned cell line from SC115 cells) estimated by [3H]thymidine incorporation into DNA and cell number reached a plateau at 10(-8) M testosterone (up to 200-fold), 10(-7) M dexamethasone (up to 30-fold) or 1 ng/ml of fibroblast growth factors (FGF; up to 50-fold).

Growth control of androgen-dependent Shionogi carcinoma cells by growth factor(s) produced from androgen-independent Shionogi carcinoma cells in a paracrine mechanism.

Androgen-dependent (SC3) and -independent (CADO21) cloned cell lines were established from androgen-dependent mouse mammary tumor (Shionogi carcinoma 115). The effects of conditioned medium (CM) collected from SC3 and CADO21 cells on the anchorage-independent growth of SC3 cells in soft agar were studied. CM prepared from SC3 cells in the absence of testosterone was unable to stimulate the growth of SC3 cells, whereas CM prepared from SC3 cells in the presence of 10(-8) M testosterone stimulated the growth of SC3 cells in a concentration-dependent manner (21 colonies at 10% and 48 colonies at 20%) and this growth-stimulatory effect was not inhibited by 10(-6) M cyproterone acetate.

[Effects of combined instillation of dapiprazole and epinephrine on human anterior chamber depth, intraocular pressure and pupil diameter].

Pilocarpine, a first choice drug for primary angle closure glaucoma (PACG), is reported to produce shallow anterior chamber and posterior synechia and consequently a small immobile pupil. In this paper, dapiprazole, a newly synthesized alpha 1 blocker, was given topically in combination with epinephrine eye drops to 15 healthy volunteers and 10 patients with PACG. In both volunteers and patients, the treated eyes revealed deeper anterior chambers, thinner lenses and significant IOP reduction after the combined instillation of dapiprazole and epinephrine.

Effect of androgen on proliferation of estrogen-responsive transformed mouse Leydig cells in serum-free culture.

We examined the effects of steroid hormones on the proliferation of transformed mouse Leydig cells (B-1) in serum-free culture condition. Among hormones examined, androgen as well as estrogen enhanced the cell proliferation rate. Hormone binding studies revealed that B-1 cells contained both androgen and estrogen receptors.

Enzyme-immunoassay for estrogen receptors in human pituitary adenomas.

We have performed an enzyme-immunoassay for estrogen receptor on 56 human pituitary adenomas and compared the results with a single point estradiol binding assay. There was a significant positive correlation between the two assays of cytoplasmic estrogen receptor (r = 0.960).

Growth-stimulatory effect of androgen-induced autocrine growth factor(s) secreted from Shionogi carcinoma 115 cells on androgen-unresponsive cancer cells in a paracrine mechanism.

Androgen-responsive (SC-3) and -unresponsive (SC-4) cloned cell lines in culture were established from an androgen-responsive mouse mammary tumor, Shionogi carcinoma 115. By using a serum-free medium [Ham's F-12:Eagle's minimum essential medium (1:1, v/v) containing 0.1% bovine serum albumin], characteristics of androgen-induced and autonomous growth factors (GFs) were examined.

Effects of estrogen and tamoxifen on secretory glycoprotein synthesis in mouse Leydig cell tumor in vivo.

Effects of estrogen and tamoxifen on the synthesis of secretory proteins were examined using estrogen-responsive mouse Leydig tumor. Estrogenization of host mice bearing the tumor (T 124958-R) resulted in the appearance of the secretory glycoprotein with a molecular weight of 34,000 which was detected by incubation of dispersed cells or minced tissues with [35S]methionine. The discontinuation of in vivo estrogenization decreased the growth rate of the tumor with the simultaneous disappearance of this secretory protein.

Autocrine regulation of cell proliferation by estradiol and hydroxytamoxifen of transformed mouse Leydig cells in serum-free culture.

We have previously reported that the cloned cell line (B-1-A-2) derived from an estrogen-responsive mouse Leydig cell tumor shows an estrogen-dependent enhancement of cell proliferation in medium supplemented with charcoal-dextran-stripped fetal bovine serum. To avoid the involvement of unknown factors present in the serum in the pathway for estrogen-dependent cell growth, the present study was designed to establish a serum-free culture system to which growth factors could be added. To this end, we subcloned B-1 cells from the parental tumor cell line.

Inhibitory and stimulatory effects of glucocorticoid on androgen-induced growth of murine Shionogi carcinoma 115 in vivo and in cell culture.

It has been generally accepted for 20 years that the growth of Shionogi carcinoma 115 (SC115) is stimulated only by androgen in vivo and in cell culture. However, we recently found that the growth of SC115 is also stimulated by pharmacological, but not physiological, doses of glucocorticoid both in vivo and in cell culture and by pharmacological doses of estrogen only in vivo. In the present study, therefore, we investigated the effect of dexamethasone on androgen-induced growth of SC115 cells in vivo and in cell culture.

A case of virilizing adrenocortical carcinoma.

A 36-year-old woman who had experienced two pregnancies consulted our hospital, because of scant menses and virilization. A 24-hour excretion of 17-ketosteroids and 17-hydroxy-corticosteroids demonstrated a decrease in 11-hydroxylase. A computed tomogram showed a huge inhomogenous tumefaction in the left adrenal.

[Regulatory mechanism of steroid hormone receptor functions].

The steroid hormone receptor has been defined as an intracellular protein which associates with the corresponding ligand in a stereospecific manner. Its binding ability and affinity have been reported to be affected by many factors such as protein kinase, SH reducing agent and molybdate. Through ligand binding, hormone-receptor complexes undergo activation process resulting in its acquisition of high affinity toward DNA.

Leupeptin inhibits the transformation of glucocorticoid receptor.

The effect of leupeptin upon the transformation of the glucocorticoid receptor was tested. When the labeled receptor was treated with heat or high salt in the presence of leupeptin, the binding to DNA-cellulose decreased in a dose-dependent manner. We observed 50% inhibition with about 40 mM leupeptin.

Both androgen and glucocorticoid induce identical secretory proteins in serum-free culture of Shionogi carcinoma 115 cells.

The effects of androgen or glucocorticoid on the induction of secretory proteins in SC-3 cells (a cloned cell line from Shionogi carcinoma 115) were examined in a serum-free medium [Ham's F-12: Eagle's minimum essential medium (1:1, v/v) containing 0.1% bovine serum albumin]. Through analysis of [35S]methionine-labeled proteins by one-dimensional (sodium dodecyl sulfate polyacrylamide) gel electrophoresis, we successfully demonstrated the production of a testosterone (10(-9)-10(-6) M)- or dexamethasone (10(-8) M)-induced secretory protein with a molecular weight of 24,000 in SC-3 cells.

Growth-stimulating effect of pharmacological doses of glucocorticoid on androgen-responsive Shionogi carcinoma 115 in vivo in mice and in cell culture.

It has been generally accepted for 20 years that the growth of Shionogi carcinoma 115 (SC115) is stimulated only by androgen. However, we recently found that the growth of SC115 cells is also stimulated by pharmacological doses of estrogen in vivo but not in cell culture. In the present study, the growth-stimulatory effect of glucocorticoid on SC115 cells was examined.

A case of von Recklinghausen's disease associated with pheochromocytoma and papillary carcinoma of the thyroid gland.

A 58-year-old woman was admitted to our hospital complaining of headache, dizziness and intermittent elevation of blood pressure. Multiple café-au-lait spots and neurofibromas had appeared on the back and the limbs since the age of 30 years. At the age of 54 years she underwent total thyroidectomy because of papillary carcinoma of the thyroid gland.

Sodium molybdate converts the RNA-associated transformed, oligomeric form of the glucocorticoid receptor into the transformed, monomeric form.

The glucocorticoid receptor from rat liver cytosol prepared in 2 ml buffer/g tissue sedimented at approximately 10 S in low salt density gradient centrifugation without molybdate. When the receptor was heated at 25 degrees C, both approximately 10 S and approximately 7 S forms were seen in low salt gradient. The approximately 10 S form was not capable of binding to DNA-cellulose and was stabilized by sodium molybdate, namely it corresponded to untransformed receptor.

Demonstration of specific dopamine receptors on human pituitary adenomas.

Dopamine receptors on human pituitary adenoma membranes were characterized using [3H] spiperone as the radioligand. The specific [3H]spiperone binding sites on prolactin (PRL)-secreting adenoma membranes were recognized as a dopamine receptor, based upon the data showing high affinity binding, saturability, specificity, temperature dependence, and reversibility. All of 14 PRL-secreting adenomas had high affinity dopamine receptors, with a dissociation constant (Kd) of 0.

Effects of estrogen and vanadate on the proliferation of newly established transformed mouse Leydig cell line in vitro.

A permanent cell line (B-1-A-2) derived from an estrogen-responsive mouse Leydig cell tumor (T 124958-R) was established in culture. Although this cell line showed estrogen-induced enhancement of cell proliferation in vitro, a moderately high concentration (10(-8) M) of estradiol was required to stimulate maximum growth. A whole cell binding assay revealed that the B-1-A-2 cells contained estrogen receptors with relatively low affinity for estradiol (Kd, 10(-9)-10(-8) M).

[Stimulation and inhibition of the growth of sex-steroid-dependent tumors].

Shionogi carcinoma 115 (SC 115) has been accepted for 20 years as a model androgen-dependent mouse mammary tumor. However, we recently found that the growth of SC 115 in vivo is also stimulated by large doses of estrogen via the estrogen receptor. In the present study, the action mechanisms involved in the growth stimulation of SC 115 were examined using a cloned cell line (SC-3) derived from the SC 115 tumor.

Growth-stimulating effect of pharmacological doses of estrogen on androgen-dependent Shionogi carcinoma 115 in vivo but not in cell culture.

Shionogi carcinoma 115 (SC115) had been accepted for 20 years as an androgen-dependent mouse mammary tumor, the growth of which is stimulated only by androgen. However, we very recently found that the growth of SC115 tumors in vivo is stimulated not only by physiological doses of androgen but also by pharmacological doses of estrogen through the estrogen receptor system. In the present study, the growth-stimulative effect of estrogen on an androgen-dependent cloned cell line (SC-3) derived from SC115 cells, which showed androgen- and estrogen-dependent growth in vivo, was examined in vitro.

Biological and biochemical characterization of estrogen-dependent mouse Leydig cell tumors.

Leydig cell tumors formed in BALB/c mice were found to be able to be transplanted subcutaneously in the same strain. One of the sublines, called T 22137, showed growth inhibition in response to estrogenization of host mice. The other subline (T 124958-O), which was originally classified as an estrogen-independent line, was observed to contain the low-affinity estradiol binding component in the cytosol fraction.

Action mechanisms of physiological doses of androgen or pharmacological doses of estrogen in growth stimulation of Shionogi carcinoma 115 in mice.

Shionogi carcinoma 115 (SC115) had been accepted for 20 yr as an androgen-dependent mouse mammary tumor. However, we recently found that the growth of SC115 tumors in vivo is also stimulated by pharmacological doses of estrogen through estrogen receptor. In the present study, action mechanisms of androgen or high doses of estrogen in the growth stimulation of SC115 were examined using a cloned cell line (SC-3) derived from the SC115 tumor.