Gonadotropin-releasing Hormone Research Articles

Reproductive disorders can result from a defective action of the neuropeptide gonadotropin-releasing hormone (GnRH), the master regulator of reproduction. We have previously shown that SELENOT, a newly-described thioredoxin-like selenoprotein highly expressed in endocrine and neuroendocrine cells, plays a role in hormone secretion and neuroprotection. However, whether SELENOT is involved in neuro-endocrine regulations in vivo is totally unknown. We found that SELENOT deficiency in the brain impaired sexual behavior, leading to a decline in fertility in both male and female mice. Biochemical and histological analyses of the gonadotrope axis of these mice revealed a higher expression of GnRH, which is associated with circulating luteinizing hormone (LH) excess, and elevated steroid hormones in males and a polycystic ovary syndrome (PCOS)-like phenotype in females. In addition, SELENOT deficiency impaired LH pulse secretion in both male and female mice. These alterations are reverted after administration of a GnRH antagonist. Together, our data demonstrate for the first time the role of a selenoprotein in the central control of sexual behavior and reproduction, and identify a new redox effector of GnRH neuron activity impacting both male and female reproductive function.

Prenatal androgen excess (PNA), an etiologic factor for polycystic ovary syndrome (PCOS), is implicated in programming long-term reproductive deficits in females such as anovulation, subfertility, and hyperandrogenism. Impaired steroid hormone feedback is a key neuroendocrine feature suspected to underpin the development of reproductive dysfunction in both clinical PCOS and in PNA mice exposed to dihydrotestosterone during late gestation. PNA is suspected to act in the brain to programme the impaired sensitivity of the gonadotropin-releasing hormone (GnRH) neuronal network to progesterone negative feedback, centrally dysregulating the hypothalamic-pituitary-ovarian axis (HPO) controlling reproduction. To test the hypothesis that androgen-sensitive neurons mediate PNA programming, we generated PNA female mice with a neuron-specific deletion of androgen receptors (NeurARKO) using Cre-lox transgenics. Following confirmation of embryonic AR deletion, PNA NeurARKO females were reproductively phenotyped and assessed for changes in progesterone receptor (PR) expression in the brain. PNA-induced reproductive traits including delayed pubertal onset, acyclicity, altered ovarian morphology, and subfertility were not different between NeurARKO and wild-type (WT) mice. In contrast, downregulation of PR expression in PNA WT mice was protected against in PNA NeurARKO mice. Together, these findings suggest that while neuronal AR may contribute to PCOS-like impaired sensitivity to progesterone feedback, their deletion alone is insufficient to rescue reproductive dysfunction associated with PCOS.

Risk of cardiometabolic disease increases in women transitioning to postmenopause, during which estradiol declines universally. Most of these women experience fragmentation of sleep due to nocturnal hot flashes, without a reduction in total sleep time. We examined the independent impact of estradiol suppression, sleep, and their combination on cardiometabolic outcomes categorized as satiety and hunger, lipid profile, cardiac vital signs, and glucoregulation. Participants completed 5-night inpatient studies under eucaloric conditions, once during mid-follicular phase/estrogenized and again under estrogen suppressed conditions, using the same experimental protocol both times. For all participants, sleep was unfragmented the first two nights and then experimentally fragmented without reducing total sleep time the next three nights. Inpatient Intensive Physiological Monitoring research facility. 38 healthy premenopausal women. Clinical experimental induced menopause model including gonadotropin-releasing hormone agonist-induced hypoestrogenism and sleep fragmentation. Leptin and satiety. Estradiol suppression significantly decreased leptin and increased lipid profiles (FDR-adjusted p≤0.05). Sleep fragmentation significantly increased heart rate (FDR-adjusted p=0.002) and trended to increase fasting glucose (FDR-adjusted p=0.08). Estradiol suppression and sleep fragmentation worsened individual cardiometabolic outcomes by (median, IQR) 4.0% (1.5%, 6.3%) from normalized baseline values. Sleep fragmentation worsened a composite cardiometabolic index derived from individual clinical cardiometabolic measures by an additional 103% over estradiol suppression alone. Independent of aging, there are significant adverse changes in cardiometabolic health induced by core components of the transition to postmenopause, including novel effects of sleep fragmentation, a modifiable target.

Purpose: Androgen deprivation therapy (ADT) for prostate cancer (PCa) is associated with cardiovascular (CV) morbidity, yet the biological basis remains unclear. Recent studies have yielded conflicting results regarding the CV safety of gonadotropin releasing hormone (GnRH) agonists versus antagonists. Re lugolix Ve rsus L e u prolide Cardiac T r i al (REVELUTION, NCT05320406) was designed to test the hypothesis that ADT-associated CV risk is mediated by accelerated coronary atherosclerosis and is more prominent with the GnRH-agonist leuprolide compared with the GnRH-antagonist relugolix. Methods: This prospective three-arm trial enrolled men with treatment-naïve, localized PCa pursuing pelvic radiotherapy (RT) alone or with concomitant ≥ 6 months ADT. Patients receiving ADT were randomized 1:1 to either leuprolide vs relugolix. Patients receiving RT alone without ADT served as a control. Primary endpoint was change in total coronary artery plaque volume (TPV), measured by prospective coronary CT angiography completed at baseline and 12 months after treatment initiation. Other outcome measures included change in non-calcified plaque volume (NCPV), calcified plaque volume (CPV), and low-attenuation plaque volume (LAPV), and incidence of major adverse CV events (MACE: stroke, myocardial infarction, coronary stent). Results: Of the 94 men enrolled from 06/2022 to 03/2024, 90 (28 RT alone, 31 RT plus leuprolide, and 31 RT plus relugolix) completed study for analysis. Median change in TPV was higher (P=.02) with leuprolide (+52.0 [19.5-159.0] mm 3 ) compared with relugolix (+25.0 [-6.0-46.0] mm 3 ) and no ADT (+13.0 [-19.0-45.0] mm 3 ). Compared with no ADT, leuprolide was associated with a significantly greater increase in TPV (estimated difference +79.1 mm 3 , P=.004), NCPV (+71.9 mm 3 , P=.001), CPV (CPV +19.9 mm 3 , P=.04), and LAPV (+5.1 mm 3 , P=.03) after adjusting for baseline plaque volume, age, and statin use. Compared with no ADT, relugolix did not result in a significant change in TPV (estimated difference +10.5 mm 3 , P=.69), NCPV (+7.2 mm 3 , P=.73), CPV (+8.9 mm 3 , P=.34), or LAPV (+1.3 mm 3 , P=.56). With a median follow-up of 23.3 (IQR 18.2-29.1) months, 3 patients (9.7%) in the leuprolide arm, 0 patients in the relugolix arm, and 1 patient (3.6%) in the no ADT arm experienced a MACE. Conclusion: ADT for PCa is associated with accelerated coronary atherosclerosis within 12 months and is significantly higher with GnRH-agonist leuprolide compared with GnRH-antagonist relugolix.

In birds, light can penetrate the cranial bones and reach deep brain regions, where non-visual photoreceptors, especially in the hypothalamus, detect spectral and photoperiodic cues. Alongside retinal photoreception, deep-brain light sensing contributes to circadian entrainment and regulates melatonin secretion by the pineal gland. These light-driven pathways modulate endocrine activity, playing a key role in muscle development. This review explores how monochromatic light-emitting diode (LED) illumination, particularly green and blue wavelengths, affects the somatotropic axis (growth hormone-releasing hormone [GHRH]-growth hormone [GH]-insulin-like growth factor 1 [IGF-1]), the gonadal axis (gonadotropin-releasing hormone [GnRH]-luteinizing hormone [LH]/follicle-stimulating hormone [FSH]-sex steroids [testosterone, estrogen, progesterone]), the thyroid axis (thyrotropin-releasing hormone [TRH]-thyroid-stimulating hormone [TSH]-thyroxine [T4]/triiodothyronine [T3]), and the hypothalamic-pituitary-adrenal (HPA) axis (corticotropin-releasing hormone [CRH]-adrenocorticotropic hormone [ACTH]-corticosterone). Green light enhances early-stage muscle growth via GHRH and IGF-1 upregulation, while blue light supports later myogenic activity and oxidative balance. Light schedules also influence melatonin dynamics, which in turn modulate endocrine axis responsiveness to photic cues. Furthermore, variations in photoperiod and exposure to artificial lights at night (ALAN) affect thyroid activity and HPA axis reactivity, influencing metabolism, thermoregulation, and stress resilience. Together, ocular and intracranial photoreception form a complex network that links environmental light to hormonal regulation and muscle growth. These insights support the strategic use of LED lighting to optimize broiler performance and welfare.

Gonadotropin-releasing hormone (GnRH) receptor antagonists in combination therapy offer a promising advancement in the medical management of uterine fibroids. While effective for symptom control, limited data exist on their impact on surgical outcomes, particularly during laparoscopic myomectomy. This case series describes the surgical findings in three patients who received preoperative Relugolix combination therapy (Relugolix-CT: relugolix-estradiol-norethisterone acetate) compared to no pretreatment. We conducted a retrospective review of 24 patients who underwent laparoscopic myomectomy over a 6-month period. Three patients received a preoperative course of Relugolix-CT for 3, 6, and 9months, respectively, while 21 patients underwent surgery without pretreatment. Blood loss was lower in the Relugolix-CT group (216.6mL ± 189.7) vs. the no-pretreatment group (354.8mL ± 131.9. Operating time was similar (148.3 vs. 148.1min), as was duration of inpatient stay (1.3 vs. 2.0days). No complications occurred in either group. Notably, in all cases with Relugolix-CT pretreatment, no distortion or fibrosis of the fibroid pseudocapsule was noted, allowing for complete resection of the fibroids. This case series suggests that preoperative Relugolix-CT does not adversely affect surgical planes or operative outcomes. Although preliminary, these findings suggest benefits for surgical optimisation and support further investigation in larger, controlled studies.

Introduction: Prostate cancer (PCa) is the most common cancer in men. Androgen deprivation therapy (ADT) is the primary systemic therapy for PCa, with over 500,000 men in the US being treated with ADT each year. Despite the most widely utilized form of ADT––gonadotropin-releasing hormone (GnRH)-agonists, such as leuprolide––being associated with accelerated coronary atherosclerosis and an increased risk of cardiovascular mortality, strategies to mitigate GnRH-agonist ADT-associated coronary atherosclerosis remain undefined. Research Question: Whether baseline statin use at the time of ADT initiation mitigates GnRH-agonist ADT-associated coronary atherosclerosis progression is unknown. Methods: This study included men with localized PCa and without coronary heart disease recruited to the REVELUTION clinical trial (NCT05320406) between 6/2022 and 3/2024. According to cancer risk, participants were treated with prostate radiation therapy (RT) alone without ADT or randomized to either RT with GnRH-agonist leuprolide or GnRH-antagonist relugolix for ≥ 6 months. The primary endpoint was change in coronary total plaque volume (ΔTPV) on CCTA from baseline to 12 months following treatment initiation. Comparisons between treatments arms were assessed according to baseline statin use with analysis of covariance and adjusted for age and baseline TPV. Results: Of 94 eligible participants, 90 (N=28, RT without ADT; N=31, RT with leuprolide; N=31, RT with relugolix) were enrolled. Mean age was 67.5 (SD 8.1) years, 26% (N=23) were Black, and 56% (N=50) were on a statin at baseline. Among leuprolide-treated participants, median 1-year ΔTPV was +101.0 [IQR 53.5-272.5] mm 3 in statin non-users and +35.0 [IQR 5.3-82.0] mm 3 in statin users (P=0.03). When compared to the no ADT arm, leuprolide treatment in statin non-users was associated with significantly increased mean-adjusted 1-year ΔTPV (+117.9 mm 3 , 95% CI 53.3-182.4, P<0.001) versus statin users (+4.9 mm 3 , 95% CI -53.7-63.5, P=0.87, P-interaction=0.002). Baseline statin use did not modify the relationship between relugolix versus no ADT and ΔTPV (P-interaction=0.25). Conclusions: Concurrent statin therapy at the time of leuprolide initiation for PCa was significantly associated with decreased coronary atherosclerosis progression when compared to those not on statins at baseline. Future prospective study should analyze the impact of concurrently initiated statin therapy on leuprolide-associated coronary atherosclerosis.

Many transgender and gender diverse (TGD) youth experience gender dysphoria which can exacerbate mental health risk. Gender-affirming medical interventions, such as pubertal suppression using gonadotropin-releasing hormone agonists (GnRHa) and gender-affirming hormone therapy (GAHT), primarily aim to alleviate gender dysphoria, with overall goals of optimizing wellbeing. Here we discuss prospective, longitudinal studies published in the last 5 years examining mental health outcomes of GnRHa and GAHT for TGD youth and young adults, contextualize these findings within the current socio-political climate, and elaborate on the need for robust and comprehensive gender-affirming care for TGD youth.

Objective: To systematically evaluate the efficacy and safety of the levonorgestrel-releasing intrauterine system (LNG-IUS) in patients with endometrial hyperplasia (EH). Methods: PubMed, Embase, the Cochrane Library, CNKI, Wanfang, CBM, and VIP were searched from inception to January 2023 for clinical trials or cohort studies involving Chinese EH patients treated with LNG-IUS alone or in combination. After screening the eligible studies, data on study population characteristics, efficacy, and safety indicators were extracted and analyzed. Results: A total of 141 studies involving 12 919 Chinese patients diagnosed with EH were included, of which 92 were randomized controlled trial (RCT) and 49 were cohort studies. The systematic review showed that after 3-12 months of LNG-IUS monotherapy, the complete response (CR) rates among Chinese patients with atypical endometrial hyperplasia (AEH) and non-atypical endometrial hyperplasia (NAEH) were 36.0%-92.3% and 23.9%-100.0%, respectively. After 12 months of treatment, the CR rate reached 84.2%-93.3%. Compared with oral progestin (OP) therapy, the CR rate after 3-12 months of LNG-IUS monotherapy was 43.6%-100.0%, while that for OP was 26.7%-97.5%. The CR rate among EH patients receiving LNG-IUS combined with gonadotropin-releasing hormone agonist (GnRHa) for 3-6 months was 31.3%-100.0%, and that for those receiving LNG-IUS combined with OP was 33.3%-93.8%. In regimens combining LNG-IUS with other drugs, LNG-IUS did not increase the incidence of adverse events (≤7.1%). Conclusion: LNG-IUS is a feasible and effective treatment option for Chinese patients with EH, offering high tolerability and low safety risks.

FSHR-GnRH bispecific vaccine suppresses the fertility of female rats.

The influence of serum luteinising hormone concentrations post GnRH agonist trigger on metaphase II oocytes in IVF/ICSI cycles.

Immunogenicity of recombinant gonadotropin-releasing hormone contraceptive vaccines in male pigs

Association of combined exposure to air pollutants during ovarian stimulation, follicular fluid metabolites, and IVF/ICSI outcomes: A prospective cohort study.

Congenital adrenal hyperplasia is the most common cause of peripheral precocious puberty in boys. Treatment with hydrocortisone usually halts the progression of peripheral precocity. However, being on this treatment, a few cases may be complicated by central precocious puberty. In such cases, treatment with a Gonadotropin-Releasing Hormone agonist (GnRHa) usually prevents further pubertal development and the acceleration of bone age. Here, we present a case of an 8-year-old boy who was diagnosed with peripheral precocious puberty due to congenital adrenal hyperplasia. He had a history of the appearance of pubic hair and phallic enlargement at 6 years of age, aggressive behavior, and hyperpigmentation. Notably, he had bilateral testicular microlithiasis and a varicocele. Despite treatment with hydrocortisone and fludrocortisone, his pubertal progression and advancement of bone age continued. Clinical and hormonal evaluation subsequently confirmed conversion to central precocious puberty. Addition of a GnRHa to his glucocorticoid and mineralocorticoid regimen successfully arrested further pubertal progression. [J Assoc Clin Endocrinol Diabetol Bangladesh, 2025;4(Suppl 1): S48]

In briefThe hypothalamus–pituitary–gonad axis integrates environmental and internal signals to tune reproductive functions. We hypothesized that in fish, Gnrh predominantly stimulates luteinizing hormone (LH) secretion, while Cck selectively regulates follicle-stimulating hormone (FSH), thereby uncovering a novel role for Cck as a metabolic gatekeeper that links reproductive activity with nutritional status.In fish, the hypothalamus–pituitary–gonad axis governs reproduction in response to environmental and internal signals. FSH regulates gonadal growth, while LH controls maturation. Gonadotropin-releasing hormone (Gnrh) plays a key role in this process, while the role of the satiety hormone cholecystokinin (Cck) is under investigation. We hypothesized that Gnrh and Cck differentially regulate tilapia LH and FSH, reflecting distinct reproductive and metabolic roles. Gnrh receptor (r) 1 was localized to FSH cells and detected only in juvenile fish, while GnRrhr3 was found in LH cells across both juvenile and mature stages. GnRH stimulation significantly increased LH release, while FSH levels showed only a moderate rise. Structural analysis revealed that Gnrhr3 exhibits more stable and rapid ligand binding and activates protein kinase A and protein kinase C (PKC) pathways, whereas Gnrhr1 signals exclusively through the PKC/Ca2+ pathway. Elevated FSH levels and gnrhr1 expression were observed during early vitellogenesis, coinciding with increased cck-rba expression in FSH cells. Cck-positive neurons originating in the brain were observed to terminate in the adenohypophysis, specifically near FSH-secreting cells. In addition, cck-rba was exclusively expressed in FSH cells, and tilapia Cck injection significantly elevated plasma FSH levels while reducing food intake, highlighting the role of Cck in linking reproduction to nutritional status. Together, these findings indicate that Gnrh predominantly regulates LH secretion via Gnrhr3, while Cck, through Cck-rba, specifically controls FSH, linking reproduction to nutritional status. Cck acts as a metabolic gatekeeper, aligning gonadal development with energy availability and ensuring reproduction when energy is sufficient.

Background and objective Ovarian endometriosis (OE), characterized by endometriotic cysts, adversely affects ovarian function and comprises in vitro fertilization and embryo transfer (IVF-ET) outcomes. Acupoint application therapy (AAT), which integrates transdermal drug delivery with acupoint stimulation, may offer therapeutic benefits; however, its underlying mechanisms remain unclear. Methods In this randomized trial, 81 IVF-ET patients were stratified into: a treatment group comprising OE patients (n=27) undergoing a gonadotropin hormone-releasing hormone (GnRH) antagonist protocol with medicated AAT, a placebo group consisting of OE patients (n=26) following an identical protocol but receiving a sham patch, and a control group, including patients with male-factor infertility (n=28) undergoing the standard protocol without additional interventions. Follicular fluid metabolomics (assessed by Ultra High-Performance Liquid Chromatography-Mass Spectrometry (UPLC-MS/MS) System)and IVF parameters were analyzed. Results Significant intergroup differences were observed (one-way ANOVA, P < 0.05). The treatment group exhibited a shorter Gn duration (9.00 ± 0.68 days) compared to the placebo group (10.62 ± 2.43 days; P < 0.05), with a duration comparable to the male-factor control group (9.32 ± 1.89 days; NS). Similarly, the total Gn dose was lower in the treatment group (2112.50 ± 483.17 IU) than in the placebo group (2549.04 ± 677.44 IU; P < 0.05), and comparable to the control group (2105.89 ± 690.24 IU; NS). Regarding IVF outcomes, the treatment group yielded more oocytes retrieved (12.41 ± 7.27) than the placebo group (8.85 ± 7.89; P < 0.05), though fewer than the control group (15.25 ± 7.77). Fertilized oocytes were also higher in the treatment group (7.59 ± 4.58) compared to the placebo group (4.46 ± 3.40; P < 0.05), but fewer than in the control group (9.21 ± 4.82). The number of transferable embryos was comparable between the treatment group (3.33 ± 2.30) and the control group (3.43 ± 2.13; NS), and significantly higher than in the placebo group (1.69 ± 1.87; P < 0.05). Furthermore, the treatment group produced more high-quality embryos (3.04 ± 1.89) than the placebo group (1.35 ± 1.99; P < 0.05), and more than the control group (2.43 ± 1.95). No significant intergroup difference was found in fertilization rates (64.40% vs. 62.90% vs. 60.90%; NS). However, the high-quality embryo rate was significantly higher in the treatment group (47.02%) compared to both the placebo (31.15%; P < 0.05) and control (29.05%; P < 0.05) groups. Finally, the treatment group demonstrated a significantly greater reduction in peri-menstrual abdominal pain scores (Δ=−1.15 ± 0.36) compared to the placebo group (Δ=−0.35 ± 0.49; F = 6.84, P = 0.01). Metabolomic analysis revealed that the steroid hormone biosynthesis pathway was the most significantly disturbed in OE patients, characterized by markedly elevated levels of key intermediates such as 17α-hydroxyprogesterne. Critically, the levels of 17α-hydroxyprogesterone exhibited a significant negative correlation with oocyte yield (r = -0.286, p = 0.012), directly linking this metabolic dysregulation to impaired clinical outcome. Furthermore, oxidative stress metabolites showed a strong positive correlation with the luteinization marker 20α-hydroxy-4-pregnen-3-one (r = 0.43, p = 0.001), suggesting a potential interaction between oxidative stress and aberrant steroidogenesis. The AAT intervention effectively normalized this dysregulated steroidogenic profile, which underpinned the observed therapeutic benefits. Conclusion AAT significantly alleviates peri-menstrual pain and enhances IVF outcomes in ovarian endometriosis patients, which may be attributed to the restoration of granulosa cell steroid metabolism, evidenced by normalized levels of 17α-hydroxyprogesterone and attenuation of oxidative stress. Clinical trial registration https://www.chictr.org.cn/ , identifier ChiCTR2200057339.

Thoracic endometriosis syndrome is a rare form of endometriosis in which endometrial tissue is thought to migrate to the lungs and, with the onset of menstruation, the ectopic foci bleed, causing a range of pulmonary manifestations. In this paper we have collected the clinical data of two patients with thoracic endometriosis syndrome, both of whom presented with haemoptysis as the first symptom and had a history of endometriosis. After 6 courses of treatment with gonadotropin-releasing hormone analogues followed by maintenance treatment with dienogest, the patients’ haemoptysis symptoms were relieved, the CT lesions in the lungs were significantly resorbed compared with the previous ones, and no recurrence was observed at long-term follow-up.

Aquaculture is the fastest growing food production industry and is becoming a vital component of the global economy to ensure food security. Fish are often raised in confined spaces, such as ponds, cages, or indoor water supply installations, in order to maximize production per unit area. At the same time, many species of fish grown in hatcheries have reproductive function disorders. These problems reduce the efficiency of aquaculture production. In some cases, it is sufficient to manipulate environmental factors such as temperature, photoperiod, salinity, and others to ensure normal spawning. However, in many fish, hormonal manipulations are required for the maturation of sexual products and subsequent spawning. The purpose of this review was to study the hormonal regulation of fish gametogenesis, as well as the main methods of stimulating producers in the factory. The paper analyzes the main problems of aquaculture production related to insufficient quantity of sexual products and low quality of breeding stock. Part of the study reveals the mechanisms of hormonal regulation of the reproductive system of fish through the brain — pituitary — gonadal axis, including the role of gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and the main stages of gametogenesis of producers. Special attention is paid to methods of hormonal stimulation of fish maturation, including the use of pituitary gland extracts, human chorionic gonadotropin (hCG), synthetic gonadotropin-releasing hormone analogues, as well as innovative hormone delivery systems with prolonged action. The prospects for further research are related to the study of the safety and optimization of the use of hormonal drugs in aquaculture.

Breast cancer (BC) is the most common malignancy in women worldwide, with incidence projected to rise, particularly among younger patients. In premenopausal women with hormone receptor-positive disease, ovarian suppression is an established component of systemic therapy, most often achieved pharmacologically with gonadotropin-releasing hormone agonists (GnRHas). Bilateral salpingo-oophorectomy (BSO) represents a surgical alternative that ensures definitive suppression, eliminates compliance issues, and is more cost-effective in the long term. Despite these advantages, BSO induces irreversible menopause, associated with vasomotor symptoms, cardiovascular morbidity, bone loss, cognitive decline, and reduced quality of life. Evidence suggests that BSO is most appropriate in selected cases, including women unable to tolerate or adhere to medical suppression, those with inadequate estradiol suppression, patients approaching natural menopause, individuals with metastatic hormone receptor-positive disease, and carriers of BRCA1 mutations, especially with triple-negative tumors. Conversely, data on its benefit in BRCA2 carriers remain limited. Overall, BSO provides oncologic outcomes comparable to medical suppression but at the cost of permanent systemic effects. The decision between surgical and medical ovarian suppression should be individualized, balancing oncologic efficacy, comorbidities, genetic background, and patient preference. Further studies are needed to define the optimal duration of medical suppression and clarify the role of BSO in hereditary breast cancer.

Effects of hormonal treatment on the expression of collagen type I, matrix metalloproteinase-1, and tissue inhibitor of metalloproteinases-1 in endometriosis.