Show simple item record

dc.contributor.advisorKoç, Ahmeten_US
dc.contributor.authorDemir, Ayşe Banu
dc.date.accessioned2015-05-22T11:58:08Z
dc.date.available2015-05-22T11:58:08Z
dc.date.issued2015-01
dc.identifier.citationDemir, A. B. (2015). Identification of doxorubicin drug resistance mechanisms by using genomic techniques. Unpublished doctoral dissertation, İzmir Institute of Technology, İzmir, Turkeyen_US
dc.identifier.urihttp://hdl.handle.net/11147/4311
dc.descriptionThesis (Doctoral)--Izmir Institute of Technology, Molecular Biology and Genetics, Izmir, 2015en_US
dc.descriptionFull text release delayed at author's request until 2016.02.03en_US
dc.descriptionIncludes bibliographical references (leaves: 71-74)en_US
dc.descriptionText in English; Abstract: Turkish and Englishen_US
dc.descriptionx, 77 leavesen_US
dc.description.abstractChemotherapy has been an important contributor for the treatment of cancer patients for a long time. The effectiveness of the therapies is influenced from the toxicity effects of the agents on normal cells and from the drug resistance. Therapeutic resistance is believed to cause the failure of the chemotherapy effectiveness in most cancer cases. Therefore, understanding the molecular mechanisms that underlie the drug resistance may contribute to increase the effectiveness of the chemotherapeutic treatment of cancer. Doxorubicin is a natural product that is widely used in treatment of various cancer types, yet many tumors have resistance against these agents. By using the budding yeast Saccharomyces cerevisiae as a model organism, we performed genome-wide screenings to identify the genes that cause resistance against this agent. Overexpression of CUE5, AKL1, CAN1, YHR177W and PDR5 genes have been identified to cause resistance against Doxorubicin at higher concentrations than the identified toxic level. Among these genes, only PDR5 overexpression was found to have cross-resistance to Cisplatin. Real-time PCR and microarray analysis for these genes were also performed. Upon 80μM Doxorubicin treatment for 2 hours, none of the CUE5, AKL1, CAN1, YHR177W and PDR5 genes showed expression changes compared to their correponding untreated wild-type status. Therefore, overexpression of these genes may not be a physiological response of yeast cells against Doxorubicin. Genome-wide microarray analysis showed changes in several cellular and biological functions upon Doxorubicin treatment. Identified genes mainly function in general stress response related events such as, filamentous growth, protein ubiquitination, autophagy, changes in membrane transportation and metabolic processes.en_US
dc.language.isoengen_US
dc.publisherIzmir Institute of Technologyen_US
dc.rightsinfo:eu-repo/semantics/embargoedAccessen_US
dc.subjectDoxorubicinen_US
dc.subjectCancer drug resistanceen_US
dc.subjectSaccharomyces cerevisiaeen_US
dc.titleIdentification of doxorubicin drug resistance mechanisms by using genomic techniquesen_US
dc.title.alternativeDoksorubisin dirençlilik mekanizmalarının genomik yöntemlerle tespit edilmesien_US
dc.typedoctoralThesisen_US
dc.contributor.authorIDTR190238en_US
dc.contributor.departmentIzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.relation.publicationcategoryTezen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record