Thesis Type: Postgraduate
Institution Of The Thesis: Uludağ Üniversitesi, Turkey
Approval Date: 2012
Thesis Language: Turkish
Student: ELİF ERTÜRK
Supervisor: GÜLŞAH ÇEÇENERAbstract:
Breast cancer is the type of cancer most frequently seen among women in the world. Recently understanding the functions of microRNAs and their roles in cancer progression has been providing expectations for understanding the molecular pathology of breast cancer and developing new molecular targeted therapies.Samples were analyzed for the presence and differential expression of 14 miRNAs (miR-21, miR-155, miR-145, let-7a, miR-10b, miR-125b, miR-221, miR-222, miR-205, miR-126, miR-206, miR-200c, miR-31 and miR-335) known to be related to diagnosis, prognosis and drug resistance of breast cancer. Expression profiles of these miRNAs were evaluated for 60 familial and/or early-onset breast tumor and 20 non-tumor tissues of patients. In order to analysis of the data in the study Independent Samples t Test, Kaplan Meier Analysis, Linear Regression Analysis, Pearson Chi-square and Fishers Exact Test were performed. According to these analysis, let-7a and miR-335 were significantly down-regulated in patients with BRCA mutations in early-onset and/or or familial breast cancer cases. In the same time, these decrease evaluated association with tumor growth and metastasis. It was found significant as statistically (p=0.044, p=0.022).These data will be beneficial for evaluation of let-7a and miR-335 expression levels to obtain information about aggressiveness of tumor and metastasis risk in early onset and/or familial breast cancer patients with BRCA mutation. In addition, these results will contribute similar therapy approaches in other breast cancer patients, thus, patients survival rates and quality of their life may be improved. Moreover, our findings will be useful for the determination of biomarkers on the follow-up of poor prognosis in breast cancer patients with BRCA mutation that could contribute to the international and national literature.