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PubMed1998

Differential regulation of the human 'leukemia inhibitory factor' (LIF) promoter in T47D and MDA-MB 231 breast cancer cells.

Leukemia inhibitory factor (LIF) is a pleiotropic inflammatory cytokine. A potential role for LIF in the pathogenesis of human breast cancer was recently indicated by the finding that LIF is produced by MDA-MB 231 breast cancer cells and that it stimulates proliferation of the T47D and MCF-7 breast cancer cell lines. Despite its role as a possible therapeutic target in breast cancer, the transcriptional regulation of the LIF gene in breast cancer cells has not been investigated so far. In this context, we investigated the regulation of the human LIF promoter (human LIF666-luciferase) by ovarian steroids in transient transfection assays in MDA-MB 231 and T47D cells. Since the MDA-MB 231 cells are devoid of both estrogen (ER) and progesterone (PR) receptors, these cells were co-transfected with the respective receptor expression vector. Estradiol induced no stimulation in either T47D or ER-transfected MDA-MB 231 cells. Treatment with the progesterone agonist MPA (medroxy-progesterone acetate) resulted in induction of LIF transcription in PR-transfectant MDA-MB 231 cells, while it had no effect in T47D cells. Both PR isoforms (PR-B and PR-A) were effective in inducing the LIF promoter in MDA-MB 231 cells, and this effect was inhibited by the progestin antagonist RU 486. The stimulatory effect of MPA was maintained on deletion constructs (h274LIF-Luc, h148LIF-Luc and h82LIF-Luc), indicating that 82 bp are sufficient to mediate this effect. Our results indicate that the LIF promoter is transcriptionally active in human breast cancer cells and its activity can be modulated by progestins and anti-progestins in cells expressing the LIF protein, which might have therapeutic implications.

Breast Neoplasms↗
PubMed2003

Induction of apoptosis in nasal polyp fibroblasts by glucocorticoids in vitro.

OBJECTIVE: To examine the possible mechanisms underlying the therapeutic mode of action of glucocorticoids (GCs) in nasal polyposis. MATERIAL AND METHODS: The effects of GCs on nasal polyps were firstly evaluated by examining the growth of fibroblasts derived from 10 nasal polyps in vitro. Subsequently, the ability of GCs to induce apoptotic cell death in fibroblasts was examined. RESULTS: Addition of betamethasone 21-phosphate (BET) at a concentration of > 1 x 10(-3) M to cell cultures inhibited cell growth in all cases examined. BET and dexamethasone 21-phosphate, but not testosterone or estradiol, caused apoptotic cell death in 2/10 nasal polyp fibroblasts, as assessed by agarose gel electrophoresis, when the cells were cultured with the agents for > 96 h. The minimum concentration of agent needed to cause apoptosis was 1 x 10(-3) M, which is half of the recommended therapeutic dose. CONCLUSION: The present findings suggest that topical application of GCs in nasal polyposis patients suppresses proliferation of fibroblasts in polyps and results in favorable modification of the clinical status of these patients.

Adult↗
PubMed2001

Estrogen replacement therapy in postmenopausal women: a study of the efficacy of estriol and changes in plasma gonadotropin levels.

The purpose of this study was to clarify the efficacy of estriol for estrogen replacement therapy in postmenopausal women with undefined symptoms and to evaluate endocrinological changes during therapy in relation to clinical outcome. Administration of 2 mg estriol in 168 postmenopausal patients was markedly effective in 22.6% of cases, effective in 45.2%, fairly effective in 14.3%, and ineffective in 17.9% of cases. The plasma concentration of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) after administration of estriol decreased significantly (p < 0.001), by 52.2% and 32.9%, respectively for markedly effective cases, and by 39.1% and 48.0% for effective cases. In contrast, the plasma estradiol concentration remained unchanged. On the other hand, decreases in FSH and LH concentration were 13.9% and 5.9% for the fairly effective and 8.2% and 1.9% for ineffective cases, demonstrating a significantly lower decrease in plasma FSH and LH levels than in the markedly effective and effective cases (p < 0.001). For cases showing side-effects, the plasma FSH and LH levels decreased by 52.0% and 64.3%, respectively, whereas the plasma estradiol level remained unchanged. In conclusion, the efficacy of estriol was significantly correlated to the degree of decrease in plasma FSH and LH levels in patients with undefined symptoms. In addition, efficacy appeared to be correlated to the incidence of side-effects. The degree of reduction of FSH (39.1-52.2%) and LH (48.0-64.3%) from the baseline may possibly be used as a guide to the therapeutic hormone levels during HRT. The present results suggest that plasma gonadotropin levels could be a useful indicator in the management of patients undergoing estrogen replacement therapy.

Biomarkers↗
PubMedDate not supplied

[Breast histologic changes in female rats treated with sex steroids].

OBJECTIVE: To evaluate the association of histologic changes in the breasts of female rats undergoing therapy with sex steroids. METHODS: An experimental study was conducted of 40 castrated female non-pubertal rats, 20 had given birth (Group B) and 20 had no offspring (Group A). After four weeks, these rats were randomly allocated to subgroups: A1, A2, A3, A4, A5 and B1, B2, B3, B4, B5. Steroids were given to subgroups as follows: A1 and B1--estradiol benzoate; A2 and B2--medroxyprogesterone acetate; A3 and B3--estradiol benzoate and medroxyprogesterone acetate; A4 and B4--tibolone; A5 and B5--placebo. After 10 weeks of treatment, animals were sacrificed and their mammary glands were analyzed. Histologic parameters evaluated were: epithelial cell proliferation, epithelial cells with secretory activity; and cell atypia in terminal duct units and buds or terminal alveoli. The association between microscopic analysis and diverse therapeutic regimens were analyzed by calculating the odds ratio and its respective 95% confidence interval. RESULTS: Histologic changes were observed in 29 rats: moderate hyperplasia (52.5%), hyperplastic alveolar nodule (42.5%), epithelial atypia (35%), mild hyperplasia (32.5%), secretory activity (20%) and severe hyperplasia (5%). In rats with no offspring when compared to the control, 1.3 times more hyperplastic alveolar nodules were found in the group treated with estradiol, the same was true for moderate hyperplasia in the rats that received medroxyprogesterone acetate, hyperplastic alveolar nodules and epithelial atypia in the group treated with estradiol plus medroxyprogesterone acetate. In the rats with offspring 1.3 times more secretory activity was found with estradiol. CONCLUSION: Epithelial hyperplasia and epithelial atypia with no proliferation are strongly associated to combined therapy with estradiol plus medroxyprogesterone acetate, mainly in the rats without offspring.

Animals↗
PubMedDate not supplied

Reduced levels of testosterone and dehydroepiandrosterone sulphate in the serum and synovial fluid of juvenile rheumatoid arthritis patients correlates with disease severity.

OBJECTIVE: The status of androgen levels and their significance in the pathogenesis of juvenile rheumatoid arthritis (JRA) has not been fully investigated. In the present study serum and synovial fluid (SF) from 20 JRA patients (grouped as pre-pubertal and pubertal) were analyzed for their content of testosterone, dehydroepiandrosterone (DHEA) and its sulphated conjugate DHEA-S, progesterone and 17 beta-estradiol. RESULTS: Comparison of the results from JRA patients with that of age-matched controls indicated no significant differences in progesterone and DHEA. Similarly, 17 beta-estradiol levels from the pubertal group were comparable to those of the controls; however, prepubertal patients had no detectable levels of this hormone. DHEA-S values were significantly lower in the pubertal JRA group, 1388.3 +/- 291.8 and 1663.9 +/- 354.1 nmol/l in the serum and SF, respectively (compared to 8206.6 +/- 848.12 in the serum of matching controls). These patients also presented with a much lower testosterone content in their SF than in their serum, 0.09 +/- 0.036 and 0.56 +/- 0.068 nmol/l, respectively (compared to 1.35 +/- 0.146 in the serum of corresponding controls). CONCLUSION: The data presented in this paper demonstrate for the first time an association between low androgen levels and disease in JRA patients. The significance of hypoandrogenicity with respect to the pathogenic mechanisms of arthritic disease and the possible therapeutic strategies that these imply warrants further investigation.

Adolescent↗
PubMedDate not supplied

Evaluation of a radioreceptor assay to assess exogenous estrogen activity in serum of patients with breast cancer.

A radioreceptor assay (RRA) for the determination of total estrogen activity, was set up and used to assess the possible presence of exogenous molecules with estrogen activity in serum; a comparison was made with the specific radioimmunoassay (RIA) for the endogenous estrogen 17-B estradiol (17-B-E2). The assay was first performed on sera from healthy people taking estrogens in the form of oral contraceptives or lotions for local application whose total estrogenic activity in the blood was assumed to be abnormal. The assay was then performed on serum from 98 patients with early breast cancer and 20 patients with metastasis, not undergoing hormone therapy. A higher estrogen activity was found in 2.5% of sera compared to the activity found using the RIA method which is specific for endogenous estrogen 17-B-E2, the RRA/17-B-E2 ratio being higher than 3. Increased estrogen activity was found in 10% serum samples from digoxin treated cardiopathic patients, with an RRA/17-B-E2 ratio ranging from 4.4 to 20. The RRA assay could prove useful for showing up exogenous estrogen activity from various sources (drugs, food) in sera of people in whom estrogen stimulation could be potentially dangerous (i.e. in patients with hormone-sensitive tumors). This exogenous activity could support a certain degree of neoplastic stimulation and, therefore, unfavourably condition the patients' therapeutic response.

Biomarkers, Tumor↗
PubMed1995

New treatment of atrophic acne scars by iontophoresis with estriol and tretinoin.

BACKGROUND: Common treatment of atrophic acne scars consists of invasive methods such as dermabrasion, chemopeeling, or implantation of bovine collagen. In our study a new noninvasive treatment method consisting of local iontophoresis is demonstrated. Local iontophoresis was performed with either estriol--a mainly topically active estrogen--or with tretinoin. PATIENTS AND METHODS: Eighteen women were treated with estriol iontophoresis twice weekly for a period of 3 months. In addition to photographic and clinical documentation of the skin, venous blood for determination of serum levels of prolactin and estradiol according to standard radioimmunoassay methods was obtained monthly. Tretinoin iontophoresis was performed according to the same time schedule in 28 patients (19 women and 9 men) with atrophic acne scars. RESULTS: Improvement of acne scars was observed in 93% of patients treated with tretinoin iontophoresis and in 100% of the group treated with estriol iontophoresis. No hormonal changes were noted in the estrogen group. Side effects involving the skin appeared in the tretinoin group in 4 cases and consisted of increased dryness and of retinoid dermatitis. CONCLUSION: Both treatments were shown to be clinically effective in decreasing acne scars and persistence of effects. This promising new therapeutic approach may thus replace invasive treatment methods in many patients.

Acne Vulgaris↗
PubMed1990

Effect of tamoxifen on DNA synthesis and proliferation of human malignant glioma lines in vitro.

Previous studies in our laboratory have shown that proliferation of human malignant gliomas in vitro depends in part upon the activation of protein kinase C (PKC) and, conversely, can be blocked by inhibitors of PKC. Here, we examined the effect of tamoxifen, a known PKC inhibitor, on DNA synthesis and proliferation of an established human glioma line (U138) and two low passage cultures of explanted human glioblastomas. Tamoxifen produced a profound, dose-dependent inhibition of both [3H] thymidine incorporation and cell proliferation, with a 50% effective dose of 20 ng/ml under serum-free conditions and 50 to 200 ng/ml in the presence of 10% serum. These tumors were estrogen receptor negative and showed no mitogenic response to estradiol. Furthermore, concentrations of estradiol as high as 10 micrograms/ml had no effect on the tamoxifen-induced inhibition. This suggests that the mechanism of growth inhibition by tamoxifen in these gliomas did not involve an estrogen receptor-mediated process but may instead result from its inhibition of PKC. In view of the profound effect of tamoxifen on cultured gliomas at concentrations that can safely be achieved therapeutically, further in vitro and in vivo studies of this agent are warranted.

Cell Division↗
PubMed1993

Preventive effect of beta-alanyl-L-histidinato zinc on the deterioration of bone metabolism in ovariectomized rats.

The preventive effect of beta-alanyl-L-histidinato zinc (AHZ) on the deterioration of bone metabolism was investigated in the femoral diaphysis of ovariectomized rats. AHZ (10, 30 and 100 mg/kg body weight/d) was orally administered to ovariectomized rats for 6 weeks. Ovariectomy produced a significant decrease in estradiol, calcitonin, calcium and inorganic phosphorus concentrations in the serum as compared with those from sham-operated rats. The dose of 30 and 100 mg AHZ/kg prevented any decrease in serum inorganic phosphorus concentration caused by ovariectomy. Alkaline phosphatase activity, deoxyribonucleic acid (DNA) and calcium contents in the femoral diaphysis of ovariectomized rats significantly decreased in comparison with those from sham-operated rats. These decreases were completely prevented by the dose of AHZ (10, 30 and 100 mg/kg). Electron microscopical analysis showed a rough alteration of bone matrix in the femoral diaphysis of ovariectomized rats. This alteration was clearly modified by the doses of AHZ (10, 30 and 100 mg/kg). Also, dosages of AHZ (30 and 100 mg/kg) restored the atrophy of osteoblasts and cartilage cells caused by ovariectomy. The present study suggests that oral administration of AHZ can prevent the deterioration of bone metabolism by ovariectomy. AHZ may have a therapeutic role in the treatment of osteoporosis.

Alkaline Phosphatase↗
PubMed2006

ALCAM/CD166 protects breast cancer cells against apoptosis and autophagy.

BACKGROUND: Activated leukocyte cell adhesion molecule (ALCAM/CD166) is a 105-kDa transmembrane glycoprotein linked with cell migration and development and with cancer progression (malignant melanoma, prostate cancer and, very recently, breast cancer). This report is the first evaluation of ALCAM/CD166 in an estrogen-dependent (MCF-7) and a metastatic (MDA-MB-231) breast cancer cell line and a reference breast cell line (HBL-100). The effects of estrogen and anti-estrogen treatment, bcl-2 overexpression, and ALCAM gene silencing on ALCAM/CD166 protein concentration and cell survival were investigated. MATERIAL/METHODS: Laser scanning cytometry, confocal microscopy, and Western blotting were used for the determination of ALCAM/CD166 protein and biochemical markers of apoptosis and autophagy. RESULTS: 17-beta-estradiol increased and tamoxifen inhibited ALCAM/CD166 expression and survival of MCF-7 cells. Overexpression of the bcl2 gene in MCF-7 bcl2/neo, MDA-MB-231 bcl2/neo, and HBL-100 bcl2/neo cells significantly increased ALCAM/CD166 expression and was accompanied by decreasing MMP-2 concentrations. Appearance of the ALCAM/CD166 protein was noted in HBL-100 bcl2/neo in contrast to an almost undetectable level in HBL-100 cells. ALCAM gene silencing in MCF-7 cells decreased the concentration of BCL-2 and increased levels of apoptosis (89-kDa PARP, active caspase7) and autophagy (MAP1LC3, Beclin1) markers. CONCLUSIONS: The above results indicate that ALCAM-ALCAM interactions are crucial to the survival and primary site maintenance of breast cancer cells. Impaired expression of ALCAM/CD166 is associated with the induction of two types of programmed cell death, apoptosis and autophagy, in breast cancer cells. This adhesion molecule can therefore be regarded as a potential novel breast cancer indicator and therapeutic target.

Activated-Leukocyte Cell Adhesion Molecule↗
PubMed2006

Estrogen deficient male mice develop compulsive behavior.

BACKGROUND: Aromatase converts androgen to estrogen. Thus, the aromatase knockout (ArKO) mouse is estrogen deficient. We investigated the compulsive behaviors of these animals and the protein levels of catechol-O-methyltransferase (COMT) in frontal cortex, hypothalamus and liver. METHODS: Grooming was analyzed during the 20-min period immediately following a water-mist spray. Running wheel activity over two consecutive nights and barbering were analyzed. COMT protein levels were measured by Western analysis. RESULTS: Six-month old male but not female ArKO mice develop compulsive behaviors such as excessive barbering, grooming and wheel-running. Excessive activities were reversed by 3 weeks of 17beta-estradiol replacement. Interestingly, the presentation of compulsive behaviors is accompanied by concomitant decreases (p < .05) in hypothalamic COMT protein levels in male ArKO mice. These values returned to normal upon 17beta-estradiol treatment. In contrast, hepatic and frontal cortex COMT levels were not affected by the estrogen status, indicating region- and tissue-specific regulation of COMT levels by estrogen. No differences in COMT levels were detectable between female animals of both genotypes. CONCLUSIONS: This study describes the novel observation of a possible link between estrogen, COMT and development of compulsive behaviors in male animals which may have therapeutic implications in obsessive compulsive disorder (OCD) patients.

Animals↗
PubMed1998

Characterization of aromatase and 17 beta-hydroxysteroid dehydrogenase expression in rat osteoblastic cells.

Postmenopausal loss of 17 beta-estradiol (E2) in women is associated with decreased bone mineral density and increased susceptibility to osteoporotic bone fracture. These changes in bone status are assumed to be due to circulating levels of the hormone; therapeutic replacement of E2 can alleviate the bone disease. However, recent reports have shown that human osteoblastic (OB) cells are able to synthesize estrogens locally, via expression of the enzyme aromatase. In this study, we have characterized the expression and activity of aromatase and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) in rat OB cell lines. Aromatase activity in ROS 17/2.8, ROS 25/1, and UMR 106 cells was similar to that shown in human OB cells, with the highest levels of activity observed in the more differentiated ROS 17/2.8 cells (Vmax = 45 pmol/h/mg of protein). The rat OB cells also showed 17 beta-HSD activity, with the predominant metabolism in all three cell lines being estrone (E1) to E2. As with aromatase, the highest activity was observed in ROS 17/2.8 cells (Vmax = 800 pmol/h/mg of protein). Northern analyses indicated the variable presence of transcripts corresponding to the type 1, 2, 3, and 4 isoforms of 17 beta-HSD. Further analysis of androstenedione metabolism indicated that the net effect of aromatase and 17 beta-HSD activity varied with cell type and culture treatment. All three OB cell lines were able to synthesize E1, E2, and testosterone from androstenedione, although activity varied between OB cell types. Regulatory effects were observed with 1,25-dihydroxyvitamin D3 (positive) and dexamethasone (negative). These data suggest that local synthesis of sex hormones is an important function of OB cells and may play a key role in the modulation of bone turnover independent of circulating hormone concentrations.

17-Hydroxysteroid Dehydrogenases↗
PubMed1989

Effect of steroids and antisteroids on human meningioma cells in primary culture.

Human meningiomas are rich in progestin receptors but virtually devoid of oestrogen receptors. We have studied the hormonal sensitivity of meningioma cells in vitro during 8 days of primary culture in the presence of different steroids and antisteroids. On day 8 the thymidine labelling index (TLI) was determined as a measure of cell growth. To date 30 cultures have been established from 39 tissue specimens. 13 cultures had a TLI below 1.0 and their growth were not affected by hormones. The TLI of the other 17 cultures was 3.0 +/- 1.7 (mean +/- SD; range 1.2-7.7). Following culture in the presence of 1 and 10 nM progesterone TLI was 83 +/- 28% (n = 9) and 61 +/- 29% (n = 3) of that of the control cultures respectively. Although in individual cultures occasional differences were found, the overall values are not statistically different from 100. Similarly, 1 nM of oestradiol and testosterone had no effect on the TLI (n = 3). Tamoxifen at 1 nM increased the TLI to 138% in one culture and decreased it to 66% of the control in another. The antiprogestin mifepristone (RU 486) in concentrations of 0.1, 1.0, 10, 100 and 1000 nM decreased the TLI to 72 +/- 30; 54 +/- 20; 55 +/- 20; 59 +/- 18 and 65 +/- 10 respectively (n = 6-15; P less than 0.05 vs control). It is concluded that although a growth promoting effect of progestins on meningioma could not be shown, the therapeutic possibilities of antiprogestins warrant further investigation.

DNA Replication↗
PubMed1990

Value of endometrial biopsies and serum hormone determinations in women with infertility.

Premenstrual endometrial biopsies were performed in 324 infertile women. Their hormonal status was established in the early follicular phase of the same cycle (FSH, LH, oestradiol-17 beta, testosterone, DHEAS, TSH and prolactin, the latter two both basally and following TRH stimulation). In the luteal phase, oestradiol-17 beta and progesterone concentrations were determined three times between the fifth and tenth hyperthermic days, as was prolactin, both basally and following metoclopramide stimulation. All pregnancies occurring before January 1986 were recorded. Seventy-five per cent of the biopsies were evaluated on the expected ovulation date from the basal temperature charts, 77% according to the next onset of menstruation. Twenty-six per cent of the biopsies were out of phase, and 7% displayed abortive secretion. A significant correlation existed between endometrial profiles and the characteristics of the cycle, stimulated TSH and prolactin levels, and with testosterone and FSH concentrations. No correlation of the endometrial status with midluteal oestradiol or progesterone concentrations was found. While various hormones of both the follicular and luteal phases correlated significantly with the pregnancy rate, the same was not demonstrated for the state of endometrial biopsy. Therefore, following exclusion of organic explanations of infertility in women with biphasic cycles, the determination of progesterone and oestradiol-17 beta in the luteal phase was considered. In women with reduced concentrations of these hormones, androgens, gonadotrophins, prolactin and TSH should be determined. Endometrial biopsy is valuable only if pregnancy fails to occur, despite therapeutically normalized hormone concentrations.

Adolescent↗
PubMed1987

Mode of estrogen action on cell proliferative kinetics in CAMA-1 cells. I. Effect of serum and estrogen.

Both serum and estrogen affect cell proliferation in CAMA-1 cells. Their effects on cell cycle kinetics are being investigated with partially synchronized cells following 48 hours of serum deprivation. By comparing the growth kinetics of synchronized (serum-deprived) cells with asynchronized (normal-fed) cells, we observed that there was a delay of cell proliferation for approximately 25 hr for synchronized cells and that estrogen only induced cell proliferation in serum-supplemented culture. A serum protein (RPF), precipitated by ammonium sulfate, dialyzed in 3,500 daltons cut off membrane and reconstituted in culture medium, was shown to stimulate cell proliferation in a dose-related manner. In the absence of RPF, estrogen had no effect on cell growth and S-phase formation in serum-free medium, but significantly induced cell growth in the presence of RPF. Experiments conducted with a synchronized cell population showed that estrogen increased the proportion of G1 phase cells to enter S phase, shortened the G1 phase duration, and ultimately increased the proportion of mitotic cells per cycle. Collectively, these results show that (a) estrogen effects of cell proliferation in vitro requires a serum component, a "G1/S-promoting factor" and (b) estrogen-induced tumor growth is a result of an accelerated rate of G1/S transition and an increased number of dividing cells per cycle. The knowledge of the interaction of estrogen with the G1/S promoting factor on cell growth is of both fundamental and therapeutic importance.

Adenocarcinoma↗
PubMed2002

Human non-small cell lung tumors and cells derived from normal lung express both estrogen receptor alpha and beta and show biological responses to estrogen.

Lung cancer is becoming increasingly common in women and in the United States accounts for more female cancer deaths annually than breast cancer. Many epidemiological studies have provided evidence that women are more susceptible than men to the adverse effects of tobacco smoke. These observations suggest the possible role of estrogens in lung carcinogenesis. We report here the expression of mRNA for estrogen receptor alpha (ERalpha) and beta (ERbeta) in cultured human non-small cell lung cancer cells, cultured lung fibroblasts, and primary cultures of normal bronchial epithelium. Western analysis of ERalpha suggested that the main protein expressed in lung tumor cells is a variant, probably attributable to alternative splicing. Protein for ERbeta was found to be a mixture of full-length as well as alternatively spliced variants. beta-Estradiol produced a proliferative response in vitro in both normal lung fibroblasts and cultured non-small cell lung tumor cells. This effect was also observed in vivo. In this regard, beta-estradiol stimulated growth of the non-small cell lung tumor line, H23, grown as tumor xenografts in SCID mice. This effect was blocked by fluvestrant (ICI 182,780). In paraffin sections of non-small cell lung tumors, ERbeta immunoreactivity was localized to the nucleus, whereas ERalpha immunoreactivity was mainly localized to the cytoplasm, suggesting that both nuclear and cytoplasmic signaling may be involved in estrogenic responses in the lung. To show that the ERs found in the lung are functional, we demonstrated that beta-estradiol stimulated transcription of an estrogen response element-luciferase construct transfected in non-small cell lung tumor cell lines. Antiestrogens blocked this effect. Treatment of lung fibroblasts with beta-estradiol also increased secretion of hepatocyte growth factor by 2-fold. These results suggest that estrogen signaling plays a biological role in both the epithelium and the mesenchyme in the lung and that estrogens could potentially promote lung cancer, either through direct actions on preneoplastic or neoplastic cells or through indirect actions on lung fibroblasts. Additionally, it is possible that antiestrogens may have therapeutic value to treat or prevent lung cancer.

Animals↗
PubMed1990

[Biologic action of promestriene on the genital tract of the castrated rat].

The study assessed the activity of promestrien administered by a local vaginal route in 16 rats castrated 60 days previously. The dose used was 5 mg per day for 10 days. Following treatment, animals were sacrificed and histological analyses revealed a remarkable proliferation of the vaginal epithelium, inhibition and restored trophism of the strome, whereas no estrogen stimulus was observed at the level of uterine mucous. This confirms the exclusively local action of promestrien which does not provoke undesirable side effects on other segments of the genital tract, and allows the therapeutic use of the hormone in different gynaecological pathologies.

Animals↗