Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik

Permanent URI for this collectionhttps://hdl.handle.net/11147/9

Browse

Filters

2007 - 20103

Settings

Author: search.filters.author.Gündüz, UfukPublisher: search.filters.publisher.Taylor and Francis Ltd.

Search Results

Now showing 1 - 3 of 3
  • Article
    Citation - WoS: 16
    Citation - Scopus: 16
    Multidrug Resistance Mediated by Mrp1 Gene Overexpression in Breast Cancer Patients
    (Taylor and Francis Ltd., 2009) Abaan, Ogan Demir; Baran, Yusuf; Baran, Yusuf; Atalay, Can; Gündüz, Ufuk; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    Multidrug resistance (MDR) is a serious handicap towards the effective treatment of breast cancer patients. One of the most prevalent MDR mechanisms is through the overexpression of genes coding the proteins called Multidrug Resistance-associated Proteins (MRPs). The aim of this study was to investigate the expression of MRP1 in tumor tissues from breast cancer patients. In this study, a semi-quantitative RT-PCR approach was utilized. Our results suggest that MRP1 overexpression can mediate MDR in patients. Pre-evaluation of the level of such MDR mediators before chemotherapy can increase the efficacy of the treatment.
  • Article
    Citation - WoS: 7
    Citation - Scopus: 7
    Nilotinib Significantly Induces Apoptosis in Imatinib Resistant K562 Cells With Wild-Type Bcr-Abl, as Effectively as in Parental Sensitive Counterparts
    (Taylor and Francis Ltd., 2010) Ekiz, Hüseyin Atakan; Can, Geylani; Baran, Yusuf; Baran, Yusuf; Ekiz, Hüseyin Atakan; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    Chronic myeloid leukemia (CML) is a hematological malignancy characterized by high levels of immature white blood cells. CML is caused by the translocation between chromosomes 9 and 22 (which results in the formation of the Philadelphia chromosome) creating BCR-ABL fusion protein. Imatinib and nilotinib are chemotherapeutic drugs which specifically bind to the BCR-ABL and inhibit cancer cells. Nilotinib is more effective in this respect than imatinib. We have shown that nilotinib induces apoptosis in imatinib-resistant K562 CML cells which have the wild-type BCR-ABL fusion gene almost to the same extent as it does in the parental sensitive cells by the increase in caspase-3 enzyme activity and the decrease in mitochondrial membrane potential. This effect of nilotinib, even in low concentrations, may indicate the efficacy of the usage of nilotinib in imatinib-resistant CML with less risk of undesired cytotoxic effects in the remaining cells of the body. © 2010 W. S. Maney & Son Ltd.
  • Article
    Citation - WoS: 33
    Citation - Scopus: 35
    Upregulation of Multi Drug Resistance Genes in Doxorubicin Resistant Human Acute Myelogeneous Leukemia Cells and Reversal of the Resistance
    (Taylor and Francis Ltd., 2007) Baran, Yusuf; Baran, Yusuf; Gür, Bala; Kaya, Pelin; Ural, Ali Uğur; Avcu, Ferit; Gündüz, Ufuk; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    The major problem in the treatment of acute myeloid leukemia (AML) patients results from multidrug resistance to administered anticancer agents. Drug resistance proteins, MDR1 and MRP1, which work as drug efflux pumps, can mediate the multidrug resistance of human leukemia cells. In this study, the mechanisms of resistance to doxorubicin-induced cell death in human HL60 AML cells were examined. Continuous exposure of cells to step-wise increasing concentrations of doxorubicin resulted in the selection of HL60/DOX cells, which expressed about 10.7-fold resistance as compared to parental sensitive cells. The expression analyses of MRP1 and MDR1 drug efflux proteins in doxorubicin-sensitive and -resistant HL60 cells revealed that there was an upregulation of MRP1 gene in HL60/DOX cells as compared to parental sensitive cells. On the other hand, while there was no expression of MDR1 gene in parental cells, the expression of MDR1 gene was upregulated in HL60/DOX cells. HL60/DOX cells also showed cross-resistance to cytosine arabinoside (Ara-c). This resistance was reversed by a combination therapy of Ara-c and cyclosporine A. However, the expression levels of CD15 and CD16 surface markers were significantly decreased in HL60/DOX cells.