Immunohistochemical Analysis of Androgen Receptor in the Abdominal Glands of the Cloaca of Male Red-Bellied Newts, Cynops pyrrhogaster

1996 ◽  
Vol 13 (3) ◽  
pp. 429-433 ◽  
Author(s):  
Akira Matsumoto ◽  
Yasumasa Arai ◽  
Fumiyo Toyoda ◽  
Sakae Kikuyama ◽  
Gail S. Prins
Gut ◽  
1998 ◽  
Vol 42 (1) ◽  
pp. 112-119 ◽  
Author(s):  
I Shimizu ◽  
M Yasuda ◽  
Y Mizobuchi ◽  
Y-R Ma ◽  
F Liu ◽  
...  

Aims—To examine the effects of oestradiol and testosterone on the early carcinogenic changes expressed in rat liver from the diethylnitrosamine (DEN), 2-acetylaminofluorene (AAF), partial hepatectomy (PH) model of hepatocarcinogenesis.Methods—Preneoplastic liver lesions were evaluated using immunohistochemical analysis of glutathione-S-transferase placental form (GST-P) expression; oestrogen and androgen receptor levels were measured by radioimmunoassay.Results—Oestradiol administration to non-castrated DEN-AAF-PH treated males resulted in a decrease in the area of GST-P positive foci, while testosterone increased the serum oestradiol level and reduced the area. In males, castration alone and castration with oestradiol replacement significantly reduced the GST-P positive area, and increased the hepatic oestrogen receptor level. In DEN-AAF-PH treated females, castration with testosterone replacement was associated with a significant increase in the GST-P positive area and the hepatic androgen receptor level.Conclusion—These findings suggest that exogenous and endogenous oestradiol can suppress chemical hepatocarcinogenesis. It appears that oestrogen receptors may be involved in the inhibition of malignant transformation of preneoplastic liver cells, while androgens and androgen receptors are involved in hepatocarcinogenesis.


2018 ◽  
Vol 53 (9) ◽  
pp. 1776-1780 ◽  
Author(s):  
Nayomi Perera ◽  
Maciej Szarek ◽  
Amanda Vannitamby ◽  
Jaya Vikraman ◽  
Georgina Huan ◽  
...  

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 595-595
Author(s):  
Sahil Seth ◽  
James Crespo ◽  
Lei Huo ◽  
Alastair Mark Thompson ◽  
Elizabeth A. Mittendorf ◽  
...  

595 Background: Androgen-receptor-like (LAR) triple-negative breast cancer (TNBC) is a subtype identified using Vanderbilt’s molecular signature. LAR subtype has the lowest pCR rate for NACT among all TNBC subtypes (10% vs. 28% for TNBC in general). We launched a clinical trial to determine the effectiveness of enzalutamide and paclitaxel (ZT) in improving this poor chemo. response in the neoadjuvant setting for pts with anthracycline-refractory, androgen receptor (AR)+ TNBC (NCT02689427). However, we do not yet have a robust predictive biomarker to detect an activated AR pathway and have not seen a robust correlation between molecular LAR subtype and AR IHC staining intensity. Methods: Molecular profiling and immunohistochemical analysis of key biomarkers (LAR, Ki67, and vimentin) was performed for all pts enrolled in A Randomized triple negative breast cancer enrolling Trial to Confirm Molecular Profiling Improves Survival (ARTEMIS; NCT02276443). Patients receive 4 cycles of AC, followed by an experimental arm or standard taxane, tailored using nuclear IHC staining. IHC staining of ≥30% AR+ was used as a threshold for selection for enzalutamide combination arm. We evaluated the concordance between LAR-subtype using molecular profiling vs % AR+ cells via IHC. Results: As part of the clinical trial, tumors with ≥30% AR+ cells were classified as LAR. In addition, we used RNA profiling to assign Vanderbilt subtype scores, resulting in classification of 15 tumors as LAR+. We observed a significant correlation (r=0.75) between LAR score and %AR+ cells, with 13 of 15 LAR tumors having ≥30% AR+ cells. Among patients with high % of AR+ tumor cells, 11 received enzalutamide, with 43% (3/7) having responses (pCR or RCB-I). Conclusions: Comparison on numerical scores for Vanderbilt subtype and IHC scores suggests ≥30% AR+ IHC staining as the threshold (ppv=0.65, npv=0.98, Table) to identify the molecular LAR subtype. We observed a trend where response rate was higher in patients with ≥ AR+ IHC scores treated with enzalutamide; however, these results need confirmation in a larger cohort of patients. Clinical trial information: NCT02689427, NCT02276443. [Table: see text]


2008 ◽  
Vol 35 (12) ◽  
pp. 1121-1126 ◽  
Author(s):  
Young Jin Kim ◽  
Jae Ho Han ◽  
Hee Young Kang ◽  
Eun-So Lee ◽  
You Chan Kim

2018 ◽  
Vol 71 (3-4) ◽  
pp. 89-95
Author(s):  
Sandra Trivunic-Dajko ◽  
Jovo Bogdanovic ◽  
Sasa Vojinov ◽  
Andrejic Visnjic

Introduction. Through androgen receptors, androgens regulate prostate cellular growth and function, proliferation, differentiation, apoptosis, lipid metabolism and secretory activity, as well as development and progression of prostate cancer. Prostate cancer, and its primary glandular tissue are influenced by hormones, and it is used for therapeutic purposes. Anti-androgen treatment is carried out in patients with metastatic prostatic cancer, in order to block effects of androgens. Immunohistochemical analysis of androgen receptors in the prostate cancer tissue may help us to assume how the tumors will react to the anti-androgen therapy, if they are androgen-positive, -negative, or hormone resistant tumors. Knowledge of the presence of androgen receptors in the tumor tissue may be a prognostic indicator in histopathological analysis. The aim of this study was stereological evaluation of androgen receptor expression in patients with benign prostatic hyperplasia and in patients with prostatic cancer, before therapy. Material and Methods. Immunohistochemical analysis was carried out using anti-human androgen receptor monoclonal antibody 441. The presence and intensity of the androgen receptors were evaluated in 195 patients: 165 with benign prostatic hyperplasia and 30 with prostatic cancer using Weibel?s multi-purpose M 42 stereological test system. Material was obtained by needle biopsy or transurethral resection of the prostate. Results. All secretory cells in patients with benign prostatic hyperplasia were androgen positive, while in patients with prostatic cancer, all tumors were mostly androgen positive, some with foci of negativity. The resulting negative correlation with Gleason score and International Society of Urological Pathology grade was not statistically significant. Conclusion. Study results of stereological analysis of androgen receptors indicate that prior the therapy prostate cancer is androgendependent, with a high level of androgen receptor expression, although slightly lower compared to benign prostatic hyperplasia.


Neuroscience ◽  
2017 ◽  
Vol 340 ◽  
pp. 201-217 ◽  
Author(s):  
Md. Nabiul Islam ◽  
Yukio Takeshita ◽  
Akie Yanai ◽  
Amami Imagawa ◽  
Mir Rubayet Jahan ◽  
...  

2008 ◽  
Vol 20 (9) ◽  
pp. 95
Author(s):  
T. Hickey ◽  
A. Tuck ◽  
M. Butler ◽  
S. Jindal ◽  
T. Dodd ◽  
...  

Polycystic ovaries (PCO) are induced by pathological or pharmacological female androgen excess, but the role of the androgen receptor (AR) in the pathogenesis of PCO is unknown. We therefore tested the hypothesis that PCO have increased expression of AR or kit ligand (KITL), a cytokine that was recently identified as a candidate AR-regulated gene in the ovary (1). Immunohistochemical analysis of AR and KITL expression was performed on archival paraffin-embedded sections of 8 morphologically normal and 8 polycystic ovaries from women under the age of 40 years. Stained sections were scanned with a NanoZoomer Digital Pathology System and immunoreactivity was qualitatively assessed using a 0-3+ scale, where 3+ represents the most intense staining. Electronic images of follicles at different stages of folliculogenesis were assessed by two independent observers who were blinded to the morphology of the source ovary. Each individual ovary contributed a minimum of 1 follicle per size class and a minimum of 10 follicles per size class were analysed. AR immunoreactivity was present in granulosa cells at all stages of folliculogenesis, in thecal cells of large antral follicles, and in the ovarian stroma. Staining intensity for AR did not differ between normal and polycystic ovaries. KITL expression, summarised in Table 1, was found to be significantly elevated in the oocytes of primordial and primary follicles and in the granulosa cells of follicles at all stages of folliculogenesis. These results show that AR expression is normal in PCO but expression of an AR-regulated gene is increased, potentially due to an excess of androgen hormone that is characteristic of women with PCO. Based on the roles of KITL established by murine studies, increased expression of KITL could explain many of the features of PCO including follicle excess, hyperthecosis and abnormal androgen secretion.


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