scholarly journals Association of prostate cancer risk with snps in regions containing androgen receptor binding sites captured by ChIP-On-chip analyses

The Prostate ◽  
2011 ◽  
Vol 72 (4) ◽  
pp. 376-385 ◽  
Author(s):  
Yizhen Lu ◽  
Jielin Sun ◽  
Andrew K. Kader ◽  
Seong-Tae Kim ◽  
Jin-Woo Kim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Risk ◽  
Receptor Binding ◽  
Binding Sites ◽  
Prostate Cancer Risk ◽  
On Chip

Polymorphisms in the androgen receptor and the prostate-specific antigen genes and prostate cancer risk

The Prostate ◽  
2005 ◽  
Vol 65 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Claudia A. Salinas ◽  
Melissa A. Austin ◽  
Elaine O. Ostrander ◽  
Janet L. Stanford
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Risk ◽  
Prostate Specific Antigen ◽  
Specific Antigen ◽  
Prostate Cancer Risk

scholarly journals Genome-wide analysis of androgen receptor binding sites in prostate cancer cells

2015 ◽  
Vol 9 (6) ◽  
pp. 2319-2324 ◽  
Author(s):  
YUE CHENG ◽  
PAN YU ◽  
XIUZHI DUAN ◽  
CHUNHUA LIU ◽  
SIQI XU ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Receptor Binding ◽  
Binding Sites ◽  
Prostate Cancer Cells ◽  
Genome Wide Analysis ◽  
Genome Wide

Abstract 3412: Androgen receptor binding sites are highly mutated in prostate cancer

2018 ◽  
Author(s):  
Tunc Morova ◽  
Mehmet Gonen ◽  
Attila Gursoy ◽  
Ozlem Keskin ◽  
Nathan A. Lack
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Receptor Binding ◽  
Binding Sites

scholarly journals Cag Repeat Number in the Androgen Receptor Gene and Prostate Cancer

2012 ◽  
Vol 15 (1) ◽  
pp. 31-36 ◽  
Author(s):  
S Madjunkova ◽  
A Eftimov ◽  
V Georgiev ◽  
D Petrovski ◽  
A Dimovski ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Risk ◽  
Receptor Gene ◽  
Prostate Cancer Risk ◽  
Androgen Receptor Gene ◽  
Repeat Length ◽  
Cag Repeat ◽  
Cag Repeats ◽  
Repeat Number

Cag Repeat Number in the Androgen Receptor Gene and Prostate CancerProstate cancer (PC) is the second leading cause of cancer deaths in men. The effects of androgens on prostatic tissue are mediated by the androgen receptor (AR) gene. The 5' end of exon 1 of the AR gene includes a polymorphic CAG triplet repeat that numbers between 10 to 36 in the normal population. The length of the CAG repeats is inversely related to the transactivation function of the AR gene. There is controversy over association between short CAG repeat numbers in the AR gene and PC. This retrospective case-control study evaluates the possible effect of short CAG repeats on the AR gene in prostate cancer risk in Macedonian males. A total of 392 male subjects, 134 PC patients, 106 patients with benign prostatic hyperplasia (BPH) and 152 males from the general Macedonian population were enrolled in this study. The CAG repeat length was determined by fluorescent polymerase chain reaction (PCR) amplification of exon1 of the AR gene followed by capillary electrophoresis (CE) on a genetic analyzer. The mean repeat length in PC patients was 21.5 ±2.65, in controls 22.28 ±2.86 (p = 0.009) and in BPH patients 22.1 ±2.52 (p = 0.038). Short CAG repeats (<19) were found in 21.64% of PC patients vs. 9.43% in BPH patients (p = 0.0154). We also found an association of low Gleason score (<7) with short CAG repeat (<19) in PC patients (p = 0.0306), and no association between the age at diagnosis of PC and BPH and CAG repeat length. These results suggest that reduced CAG repeat length may be associated with increased prostate cancer risk in Macedonian men.

scholarly journals Androgen receptor polymorphisms: Association with prostate cancer risk, relapse and overall survival

1999 ◽  
Vol 84 (5) ◽  
pp. 458-465 ◽  
Author(s):  
Stephen M. Edwards ◽  
Mike D. Badzioch ◽  
Ralph Minter ◽  
Rifat Hamoudi ◽  
Nadine Collins ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Overall Survival ◽  
Androgen Receptor ◽  
Cancer Risk ◽  
Prostate Cancer Risk

Using whole-genome sequencing to implicate the androgen receptor as the predominant driver of DNA breakpoints and fusion events in prostate cancer.

2014 ◽  
Vol 32 (4_suppl) ◽  
pp. 67-67 ◽  
Author(s):  
Niall Corcoran ◽  
Geoff Macintyre ◽  
Matthew Hong ◽  
Clare Slogget ◽  
Haroon Naeem ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Whole Genome Sequencing ◽  
Genome Sequencing ◽  
Receptor Binding ◽  
Binding Sites ◽  
Whole Genome ◽  
Structural Rearrangements ◽  
Novel Gene ◽  
Close Proximity

67 Background: Structural rearrangements in cancers genomes have the potential to disrupt normal gene function and result in a selective growth advantage, either by inactivating tumour suppressors or creating novel gene fusions with oncogenic gain-of-function. Specific fusion genes identified to date are found in particular tumor types rather than being present in all cancers suggesting there are tissue-specific mechanisms underlying these events. The most well-known fusion event in prostate cancer is TMPRSS2-ERG. Recent studies have suggested that androgen receptor may play a role in the formation of TMPRSS2-ERG fusions, bringing the two loci in close proximity in the nucleus and facilitating DNA strand break and repair along with AR associated enzymes. Methods: To explore this mechanism more comprehensively, we performed whole-genome sequencing of 14 prostate cancers from seven patients as well as paired whole blood controls. Results: Across the cancer genomes we identified approximately 4,500 high confidence DNA breakpoints and found that a large proportion of these breakpoints were in close proximity to curated androgen receptor binding sites. Furthermore, when we examined breakpoints in 11 other cancers from the TCGA and ICGC projects, we identified a similar association with androgen (and estrogen) receptor binding sites specifically in hormone-dependent tumour types, suggesting a role for steroid hormone receptors in the formation of cancer driving structural rearrangements. In addition, in at least one patient, the formation of a novel gene fusion contributed directly to the lethal evolution of his tumour. Conclusions: These data suggest that the androgen receptor drives genome wide breakpoints and novel fusion events in prostate cancer.

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