No association between polymorphism in the vascular endothelial growth factor gene at position−460 and sporadic prostate cancer in the Turkish population

Onen, Ilke Hacer; Konac, Ece; Eroğlu, Muzaffer; Güneri, Çağrı; Biri, Hasan; Ekmekçi, Abdullah

doi:10.1007/s11033-006-9046-2

Cited by 30 publications

(23 citation statements)

References 36 publications

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“…The VEGF 2460C/T polymorphism was associated with oral cancer and was a candidate genetic marker for oral cancer [Ku et al, 2005]. However, there was no association between the VEGF 2460C/T polymorphism and sporadic prostate cancer in the Turkish population [Onen et al, 2008]. Similar to the Onen's result, ours also failed to show a significant relationship between patients and controls.…”

Section: Discussionsupporting

confidence: 64%

Vascular endothelial growth factor gene polymorphisms are associated with the risk of developing adenomyosis

Kang

Zhao

Liu

et al. 2009

Environ and Mol Mutagen

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Vascular endothelial growth factor (VEGF), a major mediator of angiogenesis and vascular permeability, may play a key role in the development of adenomyosis. The aim of this study was to investigate whether these four VEGF polymorphisms (-2578C/A, -1154G/A, -460C/T, and +936C/T) were associated with the risk of adenomyosis development. Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay in 174 adenomyosis patients and 199 frequency-matched control women. There were significant differences between patients and control group in allele frequencies and genotype distributions of the -2578C/A polymorphisms (P = 0.010 and 0.044, respectively). Compared with the C/C genotype, the A/A + C/A genotype could significantly modify the risk of developing adenomyosis [odds ratio (OR) = 0.64, 95% confidence interval (CI) = 0.42-0.97]. For the -1154G/A polymorphism, the allele frequencies and genotype distributions in patient group were significant different from those of the controls (P = 0.001 and 0.007, respectively). Compared with the G/G genotype, the A/A + G/A genotype could significantly decrease the risk of developing adenomyosis (OR = 0.51, 95% CI = 0.33-0.80). However, the genotype distributions and allele frequencies of the -460C/T and +936C/T polymorphisms did not significantly differ between controls and patients (all P value > 0.05). The haplotype analysis suggested that the TGA (VEGF -460/-1154/-2578) and CGA haplotypes exhibited a significant decrease in the risk of developing adenomyosis compared with the haplotype of TGC (OR = 0.64, 95% CI = 0.41-1.00; OR = 0.44, 95% CI = 0.21-0.93, respectively). The study indicated that the -2578A or -1154A allele of VEGF gene could significantly decrease the risk of adenomyosis and might be potentially protective factors for adenomyosis development.

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Section: Discussionsupporting

confidence: 64%

Vascular endothelial growth factor gene polymorphisms are associated with the risk of developing adenomyosis

Kang

Zhao

Liu

et al. 2009

Environ and Mol Mutagen

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“…Most of the studies on European populations revealed the frequency of the T allele to range between 45 and 55% (7,18,22,23). Recently published results obtained from Turkish population show that in this group the T allele occurs in "merely" 38% (24). Therefore, caution should be exercised when extrapolating our findings to other populations.…”

Section: Discussionmentioning

confidence: 65%

Genetic Risk Factors of Bronchopulmonary Dysplasia

et al. 2008

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ABSTRACT:The aim of the study was to assess the association between bronchopulmonary dysplasia (BPD) and polymorphisms of genes coding for vascular endothelial growth factor (VEGF), transforming growth factor (TGF-␤1), insulin-like growth factor (IGF-1), and 5,10-methylenetetrahydrofolate reductase (MTHFR). A sample of 181 newborns with mean gestational age of 28 wk was prospectively evaluated. Molecular analysis of TGF-␤1 Ϫ800GϾA, Ϫ509CϾT, 10TϾC, 25GϾC, VEGF Ϫ460TϾC and 405GϾC and MTHFR 677CϾT polymorphisms were performed and the number of CA repeats in the promoter region of IGF-1 gene was assessed. The frequency of all TGF-␤1, IGF-1, and MTHFR polymorphisms, as well as the frequency of VEGF 405GϾC polymorphism was similar in all groups. The newborns with Ϫ460TT and Ϫ460CT genotypes were significantly overrepresented in the BPD groups compared with the no BPD group. Multivariate analysis revealed that carrying T allele increased the risk of BPD by 9% (95%CI: 2-14%) above the baseline risk established for given gestational age, length of oxygen therapy, and sex. Based on our data from a single center, we propose that VEGF Ϫ460TϾC polymorphism may influence the risk of BPD. A n increase in survival of extremely preterm infants has been associated with an increased incidence of bronchopulmonary dysplasia (BPD) (1), which has become a major clinical challenge because of its serious health consequences. Surviving infants with BPD are at higher risk for recurrent respiratory infections, bronchial hyperreactivity, repeated hospitalizations, and neurodevelopmental abnormalities (1,2).The current consensus is that BPD is a complex disease: the interaction of a susceptible host with a multitude of external risk factors underlies its pathogenesis. It is still unclear why BPD progresses to severe disease in one group of very low birth weight (VLBW) infants but regresses spontaneously in other infants with similar clinical characteristics. This difference in BPD development may result from differences in reactions to inflammatory stimuli and varied ability to tolerate oxidative stress and inflammation. Genetic foundations for the development of BPD are implicated in twin studies, which reveal highly significant concordance rates for BPD: 3.69-fold in monozygotic and 1.4-fold in dizygotic twins (3).The criteria for selection of BPD candidate genes in the present study were their potential involvement in angiogenesis and alveolarization regulating mechanisms, as well as their involvement in free radical elimination.The first factor worth examining is vascular endothelial growth factor (VEGF). VEGF is a relatively specific endothelial cell mitogen that regulates endothelial cell differentiation and angiogenesis, and plays a central role in vascular repair. VEGF has multiple roles in vascular development and maintenance and is essential for the formation of embryonic vasculature (4,5). The absence of VEGF results in impaired fetal lung microvascular development. The VEGF gene is also a good candidate because there are a consid...

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“…These and other VEGF polymorphisms and their association with susceptibility or prognostic value were investigated in various types of cancer and other illnesses. Data have been reported for breast cancer (Krippl et al 2003;Balasubramanian et al 2007;Jacobs et al 2006;Jin et al 2005;Kataoka et al 2006;Lu et al 2005), ovarian cancer (HeXer et al 2007), gastric cancer (Nikiteas et al 2007;Tzanakis et al 2006), lung cancer (Koukourakis et al 2004;Lee et al 2005), prostate cancer (Onen et al 2007;Sfar et al 2006), bladder cancer (GarciaClosas et al 2007) and oral squamous cell carcinoma (Yapijakis et al 2007) as well as Behcet's disease, adult respiratory distress syndrome, rheumatoid arthritis and psoriatic arthritis (Butt et al 2007;Han et al 2004;Medford et al 2005;Nam et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Common single nucleotide polymorphisms in the vascular endothelial growth factor gene and colorectal cancer risk

Hofmann

Langsenlehner

Renner

et al. 2007

J Cancer Res Clin Oncol

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No association between polymorphism in the vascular endothelial growth factor gene at position−460 and sporadic prostate cancer in the Turkish population

Cited by 30 publications

References 36 publications

Vascular endothelial growth factor gene polymorphisms are associated with the risk of developing adenomyosis

Vascular endothelial growth factor gene polymorphisms are associated with the risk of developing adenomyosis

Genetic Risk Factors of Bronchopulmonary Dysplasia

Common single nucleotide polymorphisms in the vascular endothelial growth factor gene and colorectal cancer risk

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