Genetic Effects of Vascular Endothelial Growth Factor A (VEGF-A) and Its Association with Disease Progression in Breast Cancer Population of Saudi Arabia.

Ibrahim Altedlawi Albalawi,Fm Abu Duhier,Rashid Mir

doi:10.31557/apjcp.2020.21.1.139

Ibrahim Altedlawi Albalawi, Fm Abu Duhier + Show 1 more

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https://doi.org/10.31557/apjcp.2020.21.1.139

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Abstract

Aim:Previous studies have shown that vascular endothelial growth factor (VEGFA) gene variants were associated with breast cancer risk. The goal of the current study was to evaluate the genetic effects of the vascular endothelial growth factor (VEGF) on the risk of breast cancer and its association with disease progression. Methodology:This case control study was conducted on 110 Breast cancer cases and 110 gender matched healthy controls. Vascular endothelial growth factor A (VEGF-A) 1 (-460T>C) genotyping was performed using Amplification refractory mutation system PCR method. The vascular endothelial growth factor A (VEGF-A) (-460T>C) genotypes were collated with different clinicopathological features of breast cancer patients. Results:A significant difference was observed between the genotype distribution of VEGF-A (-460T>C) among breast cancer cases and gender matched healthy controls (p=0.006). The frequencies of all three genotypes CC,CT,TT reported in the breast cancer patients and sex matched healthy controls were 4.54%, 46.36% ,49.20% and 7.27%, 64.54%, 28.18% respectively. The increased susceptibility to breast cancer disease was found to be associated with VEGF (-460T>C) CC vs TT variant in codominant inheritance model OR 2.78 (0.83-9.26) RR 1.68(1.01 to 2.81) P=0.04. A significant association was reported with VEGF (-460T>C) (CC+CT vs. TT) variant in recessive inheritance model, (OR=2.45 (95% CI= (1.40-4.29), P=0.003. Our findings indicated that VEGF (-460T>C) TT genotype is associated with an increased susceptibility to breast cancer disease. Our result indicates a potential dominant effect of VEGF (-460T>C) TT genotype on susceptibility to the breast cancer disease. Conclusion:VEGF (-460T>C) TT genotype significantly increased the risk of breast cancer. VEGF-A (-460T>C) genetic ariability was significantly associated with distant metastasis of the disease. It may be a useful as predisposing genetic marker for breast cancer .Further studies with larger sample sizes are necessary to confirm our findings.

Highlights

Breast cancer is the most common malignancy in women around the world and one in 12 women in the West develops breast cancer at some point in life
The goal of the current study was to evaluate the genetic effects of the vascular endothelial growth factor (VEGF) on the risk of breast cancer and its association with disease progression
Our findings indicated that VEGF (-460T>C) TT genotype is associated with an increased susceptibility to breast cancer disease

Summary

Introduction

Breast cancer is the most common malignancy in women around the world and one in 12 women in the West develops breast cancer at some point in life. A significant increase in the incidence of breast cancer has been reported in this part of globe (Saudi Arabia), which occurs at an earlier age than in western countries. Despite this finding, low participation rates in BC screening activities have been reported among Arab women (Al Balawi et al, 2018; Mir et al, 2018). The variations in breast carcinoma incidence rates among multicultural populations suggest that etiologic factors differ in their biologic expression and impact on disease outcome The key among those factors that affect breast carcinoma development are the roles of genetics and the environment, the reproductive experience and the effects of endogenous and exogenous hormones in women, the change in immune status and host vulnerability, and the biologic determinants of breast carcinoma (Lee et al, 2018). Molecular studies have increased the understanding of the mechanisms of chemotherapy and hormone resistance, such as the role of mutations in estrogen and progesterone receptor in resistance to endocrine therapy (Cheon et al, 2002)

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