Gamze Kuser Abali

Dr

  • 89 Commercial Road, Burnet Building, Level 4

    3004 Melbourne

    Australia

20132020

Research activity per year

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Personal profile

Biography

She received her Ph.D. degree in Molecular Biology and Genetics Department from The Bogazici University, Istanbul, Turkey, in 2011. Her Ph.D. studies focused on receptor tyrosine kinase signaling pathway regulators in retina development and diabetic retinopathy. She published her findings in IOVS journal. (Kuser-Abali et al., IOVS, 2013:54). In October 2012, She joined Cinar's lab at Cedar's Cinai Medical Center, LA, USA. She carried out two independent research projects. In the first project, she demonstrated that the oncogene MYC in concert with EZH2 suppressed the expression of MST1/STK4 in a mechanism that involves DNA hypermethylation and the inhibitory histone modification. She reported her findings in Epigenetics journal (Kuser-Abali et al. Epigenetics, 9(4), 2014). In the second project, she made a seminal observation that interaction of YAP1 with androgen receptor (AR) that is also regulated by MST1/STK4 signaling play a critical role in prostate cancer progression to the castration-resistant state, which is the lethal form of this disease. The results of this investigation were published in Nature Communications (Kuser-Abali et al. Nature Commun. September 1, 2015). Then in October 2014, she continued her second postdoc in Yuan's lab at John B. Little Center for Radiaton Sciences, Harvard University. She was concentrated on studying the epigenetic contribution of p53 in determining tissue sensitivity to DNA damage in response to chemo/radiation therapy. The results of this study are under review in PNAS. The other project that she was contributed is about the critical role of physiological levels of p53 in tissue homeostasis and cancer development. The manuscript is now under revision in Nature.

Research interests

During her PhD study she focused on receptor tyrosine kinase signaling pathway regulators in retina development and diabetic retinopathy. Her PhD work enhances our understanding of the mechanisms of Müller gliosis as a response to diseases and injury, Müller cell glucose metabolism, and the development of diabetic retinopathy in the context of FGF and insulin signaling pathway negative regulations.  During her first postdoc for almost 2 years she was working on the role of Mst1/YAP pathway in castration-resistant prostate cancer development. She identified the underlying epigenetic mechanism of Mst1 silencing during prostate cancer progression and showed the crosstalk between Hippo signaling and MYC, EZH2 in prostate cancer. In her other project, she identified the link between Hippo/YAP and AR pathways. In her second postdoc, she studied the underlying mechanism of p53 contribution on determining the tissue sensitivity to DNA damage in terms of epigenetic regulation of radiosensitive organs, such as spleen, thymus, GI tract and bone marrow cells. For this purpose, epigenetic changes are examined in isolated splenocytes, thymocytes and bone marrow cells from Mdmx mutant mice and she discovered that p53 regulates the EZH2 protein stability and in turn determines the tissue sensitivity upon radiation/chemotherapy.

Research area keywords

  • Cancer Biology
  • Epigenetics
  • Radiation
  • p53 signaling
  • Hippo/YAP signaling
  • FGFR signaling

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