Sequence Variants in Estrogen Receptors and Risk for Prostate Cancer

2004 ◽  
Author(s):  
Bao-Li Chang
2005 ◽  
Vol 173 (4S) ◽  
pp. 291-292
Author(s):  
Jamie A. Cesaretti ◽  
Richard G. Stock ◽  
Nelson N. Stone ◽  
Steven Lehrer ◽  
David A. Atencio ◽  
...  

2017 ◽  
Vol 16 (4) ◽  
pp. 235-248 ◽  
Author(s):  
Matteo Russo ◽  
Linda Ravenna ◽  
Laura Pellegrini ◽  
Elisa Petrangeli ◽  
Luisa Salvatori ◽  
...  

2013 ◽  
Vol 14 (6) ◽  
pp. 347-355 ◽  
Author(s):  
E N Rogers ◽  
D Z Jones ◽  
N C Kidd ◽  
S Yeyeodu ◽  
G Brock ◽  
...  

2015 ◽  
Vol 22 (4) ◽  
pp. 519-530 ◽  
Author(s):  
Rodrigo B de Alexandre ◽  
Anelia D Horvath ◽  
Eva Szarek ◽  
Allison D Manning ◽  
Leticia F Leal ◽  
...  

We hypothesized that mutations that inactivate phosphodiesterase (PDE) activity and lead to increased cAMP and cyclic guanosine monophosphate levels may be associated with prostate cancer (PCa). We sequenced the entire PDE coding sequences in the DNA of 16 biopsy samples from PCa patients. Novel mutations were confirmed in the somatic or germline state by Sanger sequencing. Data were then compared to the 1000 Genome Project. PDE, CREB and pCREB protein expression was also studied in all samples, in both normal and abnormal tissue, by immunofluorescence. We identified three previously described PDE sequence variants that were significantly more frequent in PCa. Four novel sequence variations, one each in thePDE4B,PDE6C,PDE7BandPDE10Agenes, respectively, were also found in the PCa samples. Interestingly,PDE10AandPDE4Bnovel variants that were present in 19 and 6% of the patients were found in the tumor tissue only. In patients carrying PDE defects, there was pCREB accumulation (P<0.001), and an increase of the pCREB:CREB ratio (patients 0.97±0.03; controls 0.52±0.03;P-value <0.001) by immunohistochemical analysis. We conclude that PDE sequence variants may play a role in the predisposition and/or progression to PCa at the germline and/or somatic state respectively.


Author(s):  
J.A. Cesaretti ◽  
R.G. Stock ◽  
D.A. Atencio ◽  
J.L. Bernstein ◽  
N.N. Stone ◽  
...  

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.


2008 ◽  
Vol 29 (5) ◽  
pp. 999-1004 ◽  
Author(s):  
Yen-Ching Chen ◽  
Edward Giovannucci ◽  
Peter Kraft ◽  
David J.Hunter

2006 ◽  
Vol 9 (3) ◽  
pp. 284-292 ◽  
Author(s):  
L R Kidd ◽  
A Coulibaly ◽  
T M Templeton ◽  
W Chen ◽  
L O Long ◽  
...  

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