Canonical ErbB-2 isoform and ErbB-2 variant c located in the nucleus drive triple negative breast cancer growth.

Triple negative breast cancer (TNBC) refers to tumors that do not express clinically significant levels of estrogen and progesterone receptors, and lack membrane overexpression or gene amplification of ErbB-2/HER2, a receptor tyrosine kinase. Transcriptome and proteome heterogeneity of TNBC poses a major challenge to precision medicine. Clinical biomarkers and targeted therapies for this disease remain elusive, so chemotherapy has been the standard of care for early and metastatic TNBC.

Nuclear PDCD4 Expression Defines a Subset of Luminal B-Like Breast Cancers with Good Prognosis.

The hormone receptor-positive (estrogen and/or progesterone receptor (PR)-positive) and HER2-negative breast cancer (BC) subtype is a biologically heterogeneous entity that includes luminal A-like (LumA-like) and luminal B-like (LumB-like) subtypes. Decreased PR levels is a distinctive biological feature of LumB-like tumors. These tumors also show reduced sensitivity to endocrine therapies and poorer prognosis than LumA-like tumors.

Distribution of FMR1 and FMR2 Repeats in Argentinean Patients with Primary Ovarian Insufficiency.

The premutation state of (Fragile X Mental Retardation 1) has been associated with primary ovarian insufficiency (POI), and is the most common known genetic cause for 46,XX patients. Nevertheless, very few studies have analyzed its frequency in Latin American populations. Additionally, a relationship between alleles carrying a cryptic microdeletion in the 5'UTR of and the onset of POI has only been studied in one population.

Expression of fragile X mental retardation protein and Fmr1 mRNA during folliculogenesis in the rat.

Fragile X mental retardation protein (FMRP) belongs to a small family of RNA-binding proteins. Its absence or inactivity is responsible for fragile X syndrome, the most common cause of inherited mental retardation. Despite its ubiquitous expression, FMRP function and expression remain almost understudied in non-neuronal tissues, though previous studies on germline development during oogenesis may suggest a special function of this protein also in ovarian tissue.

Alpha-enolase: a novel autoantigen in patients with premature ovarian failure.

Objective: Although controversial, the presence of circulating antiovarian antibodies (AOA) may be considered a marker of autoimmune premature ovarian failure (POF). The purpose of the present work was to evaluate the presence of AOA in POF patients, and to identify a possible autoantigen in order to develop a reliable diagnostic tool that might help to determine the real prevalence of autoimmune POF.

Design: Non-randomised study.

Breast cyst fluids increase the proliferation of breast cell lines in correlation with their hormone and growth factor concentration.

Objective And Design: Gross cystic disease (GCD) of the breast is reported to occur in 7% of women in the developed world and, although not premalignant, is thought to be associated with an increased risk of breast cancer. Hormone and growth factor concentration levels were measured in breast cyst fluid (BCF) to correlate them with their mitogenic activity in tumour (MCF-7) or nontransformed (MCF-10A) cells.

Results: Oestradiol (E2), oestrone (E1), E2-sulfate (E2-S), E1-sulfate (E1-S) and epidermal growth factor (EGF) concentrations were, as expected, significantly higher in type I than in type II cysts, while transforming growth factor-beta 2 (TGF-beta2) showed higher levels in type II cysts.

Controversial role of inhibin alpha-subunit gene in the aetiology of premature ovarian failure.

Background: Premature ovarian failure (POF) is characterized by hypergonadotropic amenorrhoea before the age of 40. Inhibin alpha-subunit (INHalpha) gene is proposed as a candidate gene due to its role in negative feedback control of FSH.

Methods: Polymorphism -16C>T of INHalpha gene was studied in 61 POF patients and 82 controls above 40 years old (C > 40).

Screening of FSH receptor gene in Argentine women with premature ovarian failure (POF).

Diverse mutations in FSH-receptor (FSHR) gene have been described as possible cause of premature ovarian failure (POF). To investigate the presence of mutations and/or polymorphisms in FSHR gene, DNA from 20 POF, 5 of which were diagnosed as resistant ovary syndrome (ROS), and from 44 controls was isolated from peripheral lymphocytes. The complete coding sequence was analysed by PCR followed by SSCP, direct sequencing or restriction enzyme analysis.

Circulating immunoglobulins that inhibit the binding of follicle-stimulating hormone to its receptor: a putative diagnostic role in resistant ovary syndrome?

Objective: To evaluate the presence of circulating immunoglobulins that inhibit FSH binding to its receptor (Ig-FSHR) in patients with premature ovarian failure (POF).

Design: Non-randomized study. Blood sampling for determination of circulating immunoglobulins.

Acute hCG administration induces seminiferous tubule damage in the adult rat.

In order to study the early (or short time) effects of an hCG stimulation on the seminiferous tubules of the adult rat, a single dose of 100, 200 or 400 IU hCG was administered to eighty to ninety day old rats of the Sherman strain. The histological analysis revealed a tubular damage already noticeable six hours after the injection. This precocious lesion becomes more pronounced two to five days later, consisting of degeneration and hypocellularity of the germinal epithelium, margination of the chromatin in round spermatids and formation of multinuclear giant cells.

Comparison between bioactive and immunoactive luteinizing hormone (LH) in ovariectomized streptozotocin-induced diabetic rats: response to LH-releasing hormone.

The effect of streptozotocin-induced diabetes on circulating levels of immunoactive LH (I-LH) and bioactive LH (B-LH) was investigated. LH was measured in adult ovariectomized (OVX) rats before and after acute LHRH administration, with or without estradiol benzoate (Eb) treatment (10 micrograms, 48 and 24 h before experiments). I-LH and B-LH were measured in the same samples by RIA and the rat interstitial cell testosterone assay, respectively.

Effects of induced hypoprolactinemia on testicular function during gonadal maturation in the rat.

We have evaluated the effects of hypoprolactinemia during gonadal maturation in the male rat. Intact 30-day-old rats were injected daily for 10 days with three different doses of bromocriptine (0.75, 1.

Induced hypoprolactinemia and testicular steroidogenesis in man.

The effects of short-term hypoprolactinemia on the pituitary-gonadal axis were evaluated in a group of patients with untreated prostatic carcinoma. Each patient was studied prior to and during 7-day oral administrations of bromocriptine (2.5 mg q.

Effect of prolactin on the steroidogenic response of rat luteal cells.

The role of prolactin on some ovarian functions was studied in collagenase-dispersed luteal cells obtained from PMSG/hCG-primed rats. The in vitro effect of ovine prolactin (oPrl) on luteal cell function was assayed. This hormone produced a dose-dependent increase of progesterone production and an additive effect on hCG stimulation.

Effects of prolactin, bromocriptine and sulpiride on estrogen and lactogenic receptors in the rat adrenal gland.

In prepubertal male rats, the injection of bromocriptine (Br) for 10 days caused an increase in adrenal weight (Br 0.75 mg/kg BW (Br I): 2.83%; Br 1.

Ovarian dysfunction in streptozotocin-induced diabetic rats.

The effect of streptozotocin diabetes on some ovarian functions in adult rats was examined. Diabetic diestrus animals showed reduced ovary weight and lower circulating levels of progesterone. Scatchard plots of binding data derived from ovarian particulate fractions of normal and streptozotocin diabetic rats revealed the presence of one class of binding sites with high affinity for 125I-hCG.

Inhibition of follicle-stimulating hormone receptor binding by circulating immunoglobulins.

We have characterized a circulating inhibitor of FSH receptor binding found in two patients with hypergonadotropic amenorrhea and myasthenia gravis. The inhibitor behaves as an immunoglobulin according to several criteria, including precipitation by 30% ammonium sulfate, migration on DEAE-cellulose chromatography, specific binding to protein A-Sepharose, characterization as a 7S protein in sucrose density gradients, and immunoprecipitation with specific antihuman immunoglobulin G. Evidence suggests that these antibodies are directed at determinants on or near the FSH receptor, and they may be responsible for the observed clinical FSH resistance.

Development of the gonadotrophic resistant ovary syndrome in myasthenia gravis: suggestion of similar autoimmune mechanisms.

A woman with myasthenia gravis who developed hypergonadotrophic amenorrhoea was studied. This patient fulfilled all accepted criteria for the diagnosis of the gonadotrophin resistant ovary syndrome: high levels of serum LH and FSH by radioimmunoassay and urinary gonadotrophin excretion by bioassay, low serum oestradiol, lack of response to exogenous gonadotrophin and ovaries with multiple non-stimulated primordial follicles. The serum of this patient contained a substance which behaving like a gamma globulin, inhibited FSH specific binding to receptors in an in vitro system.