Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7148

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  • Book Part
    Citation - Scopus: 4
    Epigenetics of Breast Cancer: Dna Methylome and Global Histone Modifications
    (Springer, 2016) Meşe, Gülistan; Yalçın Özuysal, Özden
    Breast cancer, a heterogeneous disease comprised of tumors with different histological characteristics and clinical outcomes, is the leading cause of cancer deaths in women. Heterogeneous nature of the breast cancer demands delicate approaches to diagnose and follow the most appropriate strategy for clinical management. Based on microarray analysis of mRNA expression, four main molecular subtypes were identified: (a) luminal A, (b) luminal B, (c) basal-like, and (d) ERBB2(+). Even though molecular subtypes provided novel insights into our understanding of breast cancer heterogeneity, there is still room for improvement for better diagnostic, prognostic and therapeutic approaches. In this sense, epigenetics, specifically DNA methylation and histone modifications, have emerged as prominent candidates since several epigenetic factors were observed to be recurrently mutated in cancers including breast cancer. Recent advances in the field implicated that DNA methylation profiles and histone modifications are strongly associated with breast tumor subtypes and patient prognosis. Therefore, understanding contributions of epigenetics to breast cancer biology will lead to better diagnostic and prognostic strategies and will enable development of novel therapeutic approaches. © Springer International Publishing Switzerland 2016.
  • Article
    Citation - WoS: 12
    Citation - Scopus: 12
    Decreased Expression of Efs Is Correlated With the Advanced Prostate Cancer
    (SAGE Publications Inc., 2015) Sertkaya, Selda; Hamid, Syed Muhammad; Dilsiz, Nihat; Varışlı, Lokman
    Prostate cancer is the most frequently diagnosed malignant neoplasm in men in the developed countries. Although the progression of prostate cancer and the processes of invasion and metastasis by tumor cells are comparatively well understood, the genes involved in these processes are not fully determined. Therefore, a common area of research interest is the identification of novel molecules that are involved in these processes. In the present study, we have used in silico and experimental approaches to compare the expression of embryonal Fyn-associated substrate (EFS) between normal prostate and prostate cancer. We showed that EFS expression is remarkably downregulated in prostate cancer cells, compared to normal prostate cells. We also found that decreased expression of EFS in prostate cancer cells is due to DNA methylation. In addition, we showed that high EFS expression is important to suppress a malignant behavior of prostate cancer cells. Therefore, we suggest that EFS should be considered as a novel tumor suppressor gene in prostate cancer.
  • Article
    Citation - WoS: 9
    Citation - Scopus: 10
    The Roles of Epigenetic Modifications of Proapoptotic Bid and Bim Genes in Imatinibresistant Chronic Myeloid Leukemia Cells
    (Taylor and Francis Ltd., 2013) Bozkurt, Süreyya; Özkan, Tülin; Özmen, Füsun; Baran, Yusuf; Sunguroglu, Asuman; Kansu, Emin
    In chronic myeloid leukemia (CML), epigenetic modifications such as promoter hypermethylation and inactive histone modification are known mechanisms of drug resistance. In our study, we investigated the roles of promoter hypermethylation of BIM and BID genes and H3K27me3 histone modification on imatinib resistance. We detected higher expression levels of BIM and BID genes and lower expression levels of EZH2, EED2, SIRT1, and SUZ12 genes in imatinib-resistant K562/IMA-3 cells compared to imatinib-non-resistant K562 cells. While we determined the EZH2 and DNMT enzymes as bounded to the promoter of the BIM gene, we did not detect hypermethylation of this promoter. We also found the H3K27me3 histone modification promoter of BIM and BID genes in both cell lines. In conclusion, our results support the notion that DNA promoter methylation may be formed independently from EZH2-H3K27me3 and pro-apoptotic BIM and BID genes are not methyllated in the imatinib resistance of CML cells.