Higher risk of progressing breast cancer in Kurdish population associated to CDH1 -160 C/A polymorphism

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Farzaneh Zarei
Mohammad Nazir Menbari
Bayazid Ghaderi
Mohammad Abdi
Zakaria Vahabzadeh

Abstract

There is an increasing interest about studying possible effects of genetic polymorphisms and risk of cancer progression. E-cadherin (CDH1) involves in many important cellular processes including cell-cell interactions, cell development and genetic changes of this molecule has been associated with greater tumor metastasis. The present study was aimed to evaluate the possible role of CDH1 -160 C/A polymorphism as a potential risk factor for breast cancer in Kurdish population. This case-control study consisted of 100 breast cancer patients and 200 healthy controls. Clinicopathological findings of all individuals were reported and immunohistochemistry staining was carried out on tissue samples. The CDH1 -160 C/A genotype was determined by polymerase chain reaction- restriction fragment length polymorphism method (PCR-RFLP). CDH1 -160 C/A polymorphism was differently distributed between patient and control groups. The A allele of CDH1 -160 C/A polymorphism significantly increased in patients compared to controls. In addition we found that the A allele of this polymorphism might be a potential risk factor for progression of breast cancer in our studied population. Patients with A allele of CDH1 -160 C/A was in higher risk to progress invasive ductal carcinoma. The A allele was also correlated with high grade and stage IV and also with metastatic tumors in studied subjects. The CDH1 -160 C/A polymorphism is correlated with clinicopathologial findings of breast cancer patients. The A allele of CDH1 -160 C/A may be a risk factor for progression of breast cancer in Kurdish patients.

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How to Cite
Zarei, F., Menbari, M. N., Ghaderi, B., Abdi, M., & Vahabzadeh, Z. (2017). Higher risk of progressing breast cancer in Kurdish population associated to CDH1 -160 C/A polymorphism. EXCLI Journal, 16, 1198-1205. https://doi.org/10.17179/excli2017-843
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Original articles