Evaluation of the effects of androgen receptor gene trinucleotide repeats and prostate-specific antigen gene polymorphisms on prostate cancer

Alptekin, Davut; İzmirli, Müzeyyen; Bayazit, Yıldırım; Hu, Luleyap; Yilmaz, Mehmet Birhan; Soyupak, Bülent; Ma, Enbo; Tansug, Zuhtu

doi:10.4238/2012.may.18.1

Cited by 13 publications

(10 citation statements)

References 32 publications

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“…By contrast, some studies did not identify an association with this repetition [43, 95, 96]. Several studies reported no association between the GGC repeat lengths, the PC risk, and pathological characteristics [34], stating that there were no significant differences between cases and controls [97]. Similarly, the risk of PC and the tumor characteristics did not differ in relation to the number of GGC repeats in this study [93].…”

Section: The Androgen Receptor (Ar) Gene and Prostate Cancer Riskcontrasting

confidence: 64%

Genotyping the High Altitude Mestizo Ecuadorian Population Affected with Prostate Cancer

López‐Cortés

Cabrera-Andrade

Salazar-Ruales

et al. 2017

BioMed Research International

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Prostate cancer (PC) is the second most commonly diagnosed type of cancer in males with 1,114,072 new cases in 2015. The MTHFR enzyme acts in the folate metabolism, which is essential in methylation and synthesis of nucleic acids. MTHFR C677T alters homocysteine levels and folate assimilation associated with DNA damage. Androgens play essential roles in prostate growth. The SRD5A2 enzyme metabolizes testosterone and the V89L polymorphism reduces in vivo SRD5A2 activity. The androgen receptor gene codes for a three-domain protein that contains two polymorphic trinucleotide repeats (CAG, GGC). Therefore, it is essential to know how PC risk is associated with clinical features and polymorphisms in high altitude Ecuadorian mestizo populations. We analyzed 480 healthy and 326 affected men from our three retrospective case-control studies. We found significant association between MTHFR C/T (odds ratio [OR] = 2.2; P = 0.009), MTHFR C/T+T/T (OR = 2.22; P = 0.009), and PC. The SRD5A2 A49T substitution was associated with higher pTNM stage (OR = 2.88; P = 0.039) and elevated Gleason grade (OR = 3.15; P = 0.004). Additionally, patients with ≤21 CAG repeats have an increased risk of developing PC (OR = 2.99; P < 0.001). In conclusion, genotype polymorphism studies are important to characterize genetic variations in high altitude mestizo populations.

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Section: The Androgen Receptor (Ar) Gene and Prostate Cancer Riskcontrasting

confidence: 64%

Genotyping the High Altitude Mestizo Ecuadorian Population Affected with Prostate Cancer

López‐Cortés

Cabrera-Andrade

Salazar-Ruales

et al. 2017

BioMed Research International

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“…The principal characteristics of included studies are listed in Table 1. Genotype distribution in controls was corresponded to HWE in all but one study [18]. …”

Section: Resultsmentioning

confidence: 99%

“…On the contrary, Abha Soni et al insisted that the genotypes AA and GA of this polymorphism were significantly related to elevated risk of BPH in their study involving 120 BPH cases and 105 controls in Indians [21]. Whereas, a study by Alptekin and colleagues detected no statistically significant difference in the frequencies of genotypes or alleles of PSA -158G/A polymorphism between controls and BPH cases in Turks, suggesting that the polymorphism might not have independent influence on the disease onset [18]. …”

Section: Disscussionmentioning

confidence: 99%

Genetic association between PSA-158G/A polymorphism and the susceptibility of benign prostatic hyperplasia: a meta-analysis

Zeng

Fang

et al. 2017

Oncotarget

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Inconsistency between reported findings on the association of prostate specific antigen (PSA) gene -158G/A polymorphism with benign prostatic hyperplasia (BPH) susceptibility need a meta-analysis to obtain a more accurate conclusion. A systematic search was conducted in electronic databases for the collection of eligible studies on PSA -158G/A polymorphism and BPH susceptibility. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were then calculated. 7 case-control studies with 758 cases and 752 controls were included into the present meta-analysis. The analysis results showed no significant relationship between PSA -158G/A polymorphism and BPH susceptibility in total analysis. Interestingly, after subgroup analyses based on ethnicity and source of control, the polymorphism reduced the susceptibility of BPH in Caucasian group (AA vs. GG: OR=0.47, 95% CI=0.25-0.89; allele A vs. allele G: OR=0.68, 95% CI=0.49-0.93), but it increased the disease susceptibility in Asian (AA vs. GG: OR=1.63, 95% CI=1.02-2.60; allele A vs. allele G: OR=1.37, 95% CI=1.03-1.83) and population-based (AA vs. GG: OR=2.39, 95% CI=1.07-5.38; allele A vs. allele G: OR=1.83, 95% CI=1.26-2.65) groups. PSA-158G/A polymorphism may be an inhibitor to the incidence of BPH in Caucasians, but it is likely to be a susceptible factor in Asians.

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“…There are numerous studies on HSV-TK suicide genes, 5-FC+GCV prodrug therapy, NTR/CB1954, and nitro reductase system on prostate cancer. Several biomarkers including prostatespecific antigen (PSA), prostate-specific membrane antigen (PSMA), androgen, C-X-C chemokine receptor type 4 (CXCR4), and epithelial cell adhesion molecule (EpCAM) have been identified for prostate cancer [82][83][84] . Consequently, promoters of the aforementioned genes are incorporated into the constructs of cancer suicide genes, which are expressed in prostate cancer cells [61,65] .…”

Section: Clinical Applicationsmentioning

confidence: 99%

The war against cancer: Suicide gene therapy

2016

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Abstract:The National Cancer Institute and the American Cancer Society announced that 1.6 million new cancer cases are projected to occur in the USA in 2016. One of the most innovative approaches against cancer is suicide gene therapy, in which suicide-inducing transgenes are introduced into cancer cells. When cancer treatments target the total elimination of tumor cells, there will be no side effects for normal cells. Cancer tissues are targeted through various targeted transport methods, followed by tissue-specific enzymes converting a systemically suitable prodrug into an active drug in the tumor. Suicidal genes are delivered by transporters, such as viral and non-viral vectors, into cancer cells. Suicide gene therapeutic strategies currently pursued are herpes simplex virus thymidine kinase gene with prodrug ganciclovir, cytosine deaminase gene, carboxyl esterase/irinotecan, varicella zoster virus thymidine kinase/6-methoxypurine arabinonucleoside, nitroreductase Nfsb/5-(aziridin-1-yl)-2,4-dinitrobenzamide, carboxypeptidase G2/4-[(2-chloroethyl) (2-mesyloxyethyl)amino] benzoyl-L-glutamic acid, cytochrome p450-isofosfamide, and cytochrome p450-cyclophosphamide. The goal of this review is to summarize the different suicide gene systems and gene delivery vectors addressed to cancer cells, with a particular emphasis on recently developed systems. Finally, we briefly describe the advantageous clinical applications and potential side effects of suicide gene therapy.

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Evaluation of the effects of androgen receptor gene trinucleotide repeats and prostate-specific antigen gene polymorphisms on prostate cancer

Cited by 13 publications

References 32 publications

Genotyping the High Altitude Mestizo Ecuadorian Population Affected with Prostate Cancer

Genotyping the High Altitude Mestizo Ecuadorian Population Affected with Prostate Cancer

Genetic association between PSA-158G/A polymorphism and the susceptibility of benign prostatic hyperplasia: a meta-analysis

The war against cancer: Suicide gene therapy

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