Immunolocalization of Androgen Receptor and Estrogen Receptors in Skin Tags

2014 ◽  
Vol 38 (5) ◽  
pp. 344-357 ◽  
Author(s):  
Ola Ahmed Bakry ◽  
Rehab Monir Samaka ◽  
Mohamed Abdel Moneim Shoeib ◽  
Aziza Maher
2011 ◽  
Vol 29 (7_suppl) ◽  
pp. 168-168 ◽  
Author(s):  
R. Nunez-Nateras ◽  
E. P. Castle

168 Background: Androgens and estrogens have been shown to play an important role in normal prostate development and function as well as carcinogenesis and development of the castration resistant phenotype of disease. The aim of this study was to evaluate the effect of a simultaneous administration of an androgen receptor antagonist (bicalutamide) and a selective estrogen receptor modulator (raloxifene) on both androgen sensitive and androgen insensitive prostate cancer cell lines. Methods: Experiments were performed on LNCaP, PC3 and DU145 cell lines. Western blot was utilized for the identification of androgen and estrogen receptors (a andb) in the cell lines. Drug concentrations required to achieve IC 50 were obtained using the MTT assay; such concentrations were identified for the drugs individually and when used in combination. The effect of the drugs on apoptosis was assessed using flow cytometry. Results: Results of the IC 50 for the drugs alone and in combination by each cell line are shown in the table. An enhanced effect was observed when the drugs were used in combination in all the cell lines. It was evident that the combination of the drugs decreased the total drug required to achieve the IC50 decreases considerably. Apoptosis rates were also affected by the simultaneous administration of bicalutamide and raloxifene. The synergistic effect of the combination was reflected in the increase of the apoptosis rate in all cell lines. Conclusions: The simultaneous administration of bicalutamide and raloxifene has a synergistic effect on cell death and apoptosis of DU145, PC3 and LNCaP cell lines. The pathway(s) responsible for this observation may be independent of the androgen receptor as both AR negative cell lines were still affected by the combination over the SERM alone. [Table: see text] No significant financial relationships to disclose.


2013 ◽  
Vol 42 (5) ◽  
pp. 877-887 ◽  
Author(s):  
Shin Wakui ◽  
Masaru Shirai ◽  
Masaya Motohashi ◽  
Tomoko Mutou ◽  
Noriko Oyama ◽  
...  

2012 ◽  
Vol 58 (6) ◽  
pp. 629-635 ◽  
Author(s):  
Candela Roc^|^iacute;o GONZ^|^Aacute;LEZ ◽  
Mar^|^iacute;a Laura Muscarsel ISLA ◽  
Noelia Paola LEOPARDO ◽  
Miguel Alfredo WILLIS ◽  
Ver^|^oacute;nica Berta DORFMAN ◽  
...  

2004 ◽  
Vol 6 (3) ◽  
Author(s):  
Isabel Conde ◽  
Juan M Alfaro ◽  
Benito Fraile ◽  
Antonio Ruíz ◽  
Ricardo Paniagua ◽  
...  

Author(s):  
Cristina Aguirre-Portolés ◽  
Riley Payne ◽  
Aspen Trautz ◽  
J. Kevin Foskett ◽  
Christopher A. Natale ◽  
...  

AbstractMelanoma and most other cancers occur more frequently, and have worse prognosis, in males compared with females. Though sex steroids are thought to be involved, classical androgen and estrogen receptors are not detectable in most melanomas. Here we show that testosterone promotes melanoma proliferation by activating ZIP9 (SLC39A9), a zinc transporter that is not intentionally targeted by available therapeutics, but is widely expressed in human melanoma. This testosterone activity requires zinc influx, MAPK activation and YAP1 nuclear translocation. We demonstrate that FDA approved inhibitors of the classical androgen receptor also inhibit ZIP9, and thereby antagonize the pro-tumorigenic effects of testosterone in melanoma. In male mice, androgen receptor inhibitors suppressed growth of ZIP9-expressing melanomas, but had no effect on isogenic melanomas lacking ZIP9, nor on melanomas in females. These data suggest that ZIP9 might be effectively targeted in melanoma and other cancers by repurposing androgen receptor inhibitors that are currently approved only for prostate cancer.


2002 ◽  
Vol 35 (4) ◽  
pp. 281-286 ◽  
Author(s):  
Ya-Gai Yang ◽  
Naoji Toyota ◽  
Toyofusa Tobe ◽  
Yoshiharu Matsuno ◽  
Kaiya Takano ◽  
...  

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