Research Focus

* Our main research interest is to identify the genes targeted by BRCA1 gene.
* We are also interested in the identification of tumor-related genetic changes and the elucidation of resulting phenotypic aberrations in breast cancer.

Academic Degrees and Employment

Education:

Employment:

Graduate & Fellowship Program Affiliations

Department of Molecular Biology and Genetics

Summary of Requirements for Admission to Graduate Programs

Research Interests

Acquired or inherited mutations of tumor suppressor genes are crucial in the initiation and progression of human malignancies. The tumor suppressor gene BRCA1 (Breast Cancer Susceptibility gene 1) is responsible for a significant portion of inherited breast and ovarian cancers. It encodes a protein 1863 aminoacids. It has a zinc finger domain, two putative nuclear localization signals, a leucine zipper and a transactivation domain in the C-terminus region. This region acts as a strong transactivator. BRCA1 protein possess a number of features common to transcriptional regulatory proteins, and also several lines of evidence suggests that it has a role in maintaining the genomic integrity. These suggests that BRCA1 may regulate the expression of one or more genes, which therefore represent potential effectors of BRCA1 tumor suppressor function. Although there are several studies about the function of BRCA1, the exact biochemical and tumor suppressor function of this gene remains to be identified. Our main research interest is to identify the genes targeted by BRCA1 gene. In this line we have a mammalian cell system where BRCA1 gene expression level can be controlled. By using differential gene expression method and making subtractive cDNA libraries we will try to answer some questions about the function of BRCA1 gene. We are also interested in identifying the genetic changes in different tumor tissue types which may be the cause of the tumor formation.

Click for Yulug Lab

* B. Gur, O. Konu, S. Kir, A.R. Ozturk, B. Bozkurt, G. Ergul, I. Yulug, “A Resampling Based Meta-Analysis for Detection of Differential Gene Expression in Breast Cancer,” accepted for publication in BMC Genomics

* M. Mumcuoglu, S. Bagislar, H. Yuzugullu, H. Alotaibi, S. Senturk, P. Telkoparan, B. Gur-Dedeoglu, B. Cingoz, B. Bozkurt, U.H. Tazebay, I. Yulug, K.C. Akcali, M. Ozturk, Heterogeneity,” Plos One, vol. 5, pp. 11288–1-12 (2010) PubMed

* B. Gur, O. Konu, B. Bozkurt, G. Ergul, S. Seckin, I. Yulug, “Identification of endogenous reference genes for qRT-PCR analysis in normal matched breast tumor tissues,” Oncology Research, vol. 17, pp. 353-365 (2009) PubMed

* E. Canbay, B.Gur-Dedeoglu, B. Bozkurt, M. Karabeyoglu, B. Unal, O. Yildirim, O. Cengiz, I. Yulug, “Inhibition of focal adhesion kinase with her-2 targeted antibody pertuzumab (Omnitarg (R), 2C4) in breast cancer cells,” Gene Therapy and Molecular Biology, vol. 12, pp. 293-300 (2008) PubMed

* I. Yulug, B. Gur-Dedeoglu, “Functional Genomics in Translational Cancer Research: Focus on Breast Cancer,” Briefings in Functional Genomics and Proteomics, vol. , pp. (2008) PubMed

* N. Ozturk, E. Erdal, M. Mumcuoglu, K.C. Akcali, O. Yalcin, S. Senturk, A. Arslan-Ergul, B. Gur, I. Yulug, R. Cetin-Atalay, C. Yakicier, T. Yagci, M. Tez, M. Ozturk, Proceedings of National Academy of Sciences USA, vol. 103, pp. 2178-2183 (2006) PubMed

* A. Petenkaya, B. Bozkurt, O. Akilli-Ozturk, H.S. Kaya, B. Gur-Dedeoglu, I. Yulug, “Lack of Association Between the MDM2-SNP309 Polymorphism and Breast Cancer Risk,” Anticancer Research, vol. 26, pp. 4975-4978 (2006) PubMed

* Turk M., Dincer S., Yulug I.G., Piskin E. “In vitro tansfection of HeLa cells with temperature sensitive polycationic copolymers”. Journal of Controlled Release, 96: 325-340 (2004).  PubMed

* Sevinc A., Yannoukakos D., Konstantopoulou I., Manguloglu E., Luleci G., Colak T., Akyerli C., Colakoglu G., Tez M., Sayek I., Gerassimos V., Nasioulas G., Papadopoulou E., Florentin L., Kontogianni E., Bozkurt B., Kocabas N. A., Karakaya A.E., Yulug I.G., Ozcelik T. “Lack of Association Between RNASEL Arg462Gln Variant and the Risk of Breast Cancer”. Anticancer Research 24:2547-2549 (2004).  PubMed

* Bergamaschi D., Gasco M., Hiller L., Sullivan A., Syed N., Trigiante G., Yulug I.,  Merlano M., Numico G., Comino A., Attard M., Reelfs O., Gusterson B., Bell A.K., Heath V., Tavassoli M., Farrell P.J., Smith P., Lu X., Crook T.  “p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis”.  Cancer Cell 3:387-402 (2003).  PubMed

* Atalay A., Crook T., Ozturk M., Yulug I.G. “Identification of genes induced by BRCA1 in breast cancer cells”. Biochem. Biophys. Res. Commun. Dec 20;299(5):839-46 (2002). PubMed

* Gasco M., Bell AK., Heath V., Sullivan A., Smith P., Hiller L., Yulug I., Numico G., Merlano M., Farrell P.J., Tavassoli M, Gusterson B., Crook T. “Epigenetic inactivation of 14-3-3 sigma in oral carcinoma: association with p16 INK4a silencing and human Papillomavirus negativity “. Cancer Research  62, 2072-2076 (2002).   PubMed

* Sullivan A., Yuille M., Repellin C., Reddy A., Reelfs O., Bell A., Dunne B., Gusterson B.A., Osin P., Farrell P.J., Yulug I., Evans A., Ozcelik T., Gasco M., Crook T. “Concomitant inactivation of p53 and Chk2 in breast cancer” Oncogene  21(9):  1316-1324 (2002).   PubMed

* Marin M.C., Jost A.J., Brooks L.A., Irwin M.S., O’Nions J., Tidy J.A., James N., McGregor J.M., Harwood C.A., Yulug I.G.,  Vousden K.H., Allday M.J., Gusterson B., Ikawa S., Hinds P.W., Crook T.,  Kaelin Jr W.G..  “A common polymorphism acts as an intragenic modifier of mutant p53 behaviour”.  Nature Genetics 25:  47-54 (2000). PubMed