Vascular endothelial growth factor (VEGF) polymorphism and increased risk of epithelial ovarian cancer
Introduction Angiogenesis (AG) is essential for epithelial ovarian cancer (EOC) development. Vascular endothelial growth factor (VEGF), encoded by the VEGF gene, and endostatin, the product of the COL18A1 gene, act as a potent promoter and an inhibitor of AG, respectively. In the present study, we t...
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Veröffentlicht in: | Journal of cancer research and clinical oncology 2015-01, Vol.141 (1), p.69-73 |
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Sprache: | eng |
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Zusammenfassung: | Introduction
Angiogenesis (AG) is essential for epithelial ovarian cancer (EOC) development. Vascular endothelial growth factor (VEGF), encoded by the
VEGF
gene, and endostatin, the product of the
COL18A1
gene, act as a potent promoter and an inhibitor of AG, respectively. In the present study, we tested whether
VEGF
C936T and
COL18A1
D104N polymorphisms alter the risk of EOC.
Methods
Genomic DNA from 131 EOC patients and 137 controls were analyzed by polymerase chain reaction and restriction fragment length polymorphism methods. The differences between groups were analyzed by
χ
2
or Fisher’s exact test and logistic regression analysis.
Results
The frequency of the
VEGF
936CC genotype was higher in patients than in controls (84.8 % vs. 75.3 %,
P
= 0.03). Individuals with respective genotypes had a 1.98 (95 % CI 1.04–3.78)-fold increased risk of EOC than those with the remaining genotypes. An excess of
VEGF
936CC plus
COL18A1
DN genotype was seen in patients when compared to controls (48.6 % vs. 30.5 %); however, only a tendency toward a statistically significant difference in genotype frequencies was found in the study (
P
= 0.06), reflecting a trend toward an increased risk of 2.44 for EOC in carriers of the combined genotype.
Conclusion
Our data present, for the first time, preliminary evidence that
VEGF
C936T alone or combined with the
COL18A1
D104N polymorphism of AG constitutes an important inherited EOC determinant. |
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ISSN: | 0171-5216 1432-1335 |
DOI: | 10.1007/s00432-014-1786-0 |