Işık G. Yuluğ



Faculty Member

Office: SB-306
Phone: +90 312 290 2506
E-mail: yulug@fen.bilkent.edu.tr
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Dr. Isik G. Yulug is Associate Professor at Bilkent University, Molecular Biology and Genetics. She has been the Chair of the Department between 2014-2017. Dr. Yulug graduated from Hacettepe University, Faculty of Science, Department of Biology, Ankara, Turkey. She received her master’s degree from Hacettepe University, Faculty of Medicine, Medical Biology Department in 1990. She then earned her PhD degree in molecular genetics at University of London, the Imperial College of Science, Technology and Medicine in 1995. She worked at University of London, Ludwig Cancer Institute, London and M.D. Anderson Cancer Research Center. She was awarded with NATO PhD fellowship by TUBITAK. She is a recipient of Lawley Scholarship by University of London, the Best Scientific Work Award of the World Society for Breast Health and the L’Oreal-UNESCO Women in Science Award. She joined to the Bilkent University in 1996. She acted as assistant chair between 2001-2007 and as a deputy chair in 2007-2008. She has been the member of Science Faculty Board since 2002, member of the Board of directors in Graduate School of Engineering and Science, Bilkent University since 2012. She served as Council Member in European Association for Cancer Research and has been representing Turkey in the council for four years. She worked as an Elected Steering Committee Member for the Research Networking Program on Frontiers of Functional Genomics in European Science Foundation since for four years. She is currently serving as a member of UNESCO Bioethics Committee member in Turkey.

Her group has concentrated working on the identification, expression profiling, and epigenetic mechanisms of the genes involved in initiation and progression of human malignancies especially in breast cancer. Her articles published in citation index journals received over 1500 citations.


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.

Key Publications

Ozturk, N., Erdal, E., Mumcuoglu, M., Akcali, K. C., Yalcin, O., Senturk, S., Arslan-Ergul, A., Gur, B., Yulug, I., Cetin-Atalay, R., Yakicier, C., Yagci, T., Tez, M., & Ozturk, M. (2006). Reprogramming of replicative senescence in hepatocellular carcinoma-derived cells. Proceedings of the National Academy of Sciences of the United States of America, 103(7), 2178–2183.

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. (2003). p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis. Cancer cell, 3(4), 387–402.

Gasco, M., Bell, A. K., Heath, V., Sullivan, A., Smith, P., Hiller, L., Yulug, I., Numico, G., Merlano, M., Farrell, P. J., Tavassoli, M., Gusterson, B., & Crook, T. (2002). Epigenetic inactivation of 14-3-3 sigma in oral carcinoma: association with p16(INK4a) silencing and human papillomavirus negativity. Cancer research, 62(7), 2072–2076.

Marin, M. C., Jost, C. A., 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, W. G., Jr (2000). A common polymorphism acts as an intragenic modifier of mutant p53 behaviour. Nature genetics, 25(1), 47–54.