Marwa Taya

I earned both my bachelor's and master's degrees in biological sciences from Florida Atlantic University. Furthermore, I pursued my PhD studies at Tel Aviv University in Israel under the supervision of Professor Ido Wolf and Dr. Tami Rubinek. During my 4 years of PhD studies, I had the opportunity to work on two projects. First, I investigated the relationship between ESR1 mutations and chemotherapy resistance. I focused on the two most common mutations, D538G and Y537S, and showed, for the first time, that mutated cells are resistant to chemotherapy treatments. Subsequently, I examined the possible mechanisms leading to this resistance and found, using a diverse array of methods, that the JNK pathway is activated in cells expressing the mutated ER, followed by the upregulation of MDR1, the major protein mediating resistance to chemotherapy, in both cell lines and clinical samples.  In my second project, I studied the metabolic pathways associated with the aggressive disease phenotype of cells harboring ESR1 mutations. Using mass spectrometry analysis (in collaboration with the Sekler lab at the University of Ben Gurion), I was able to show an increase in SLC25A15, a mitochondrial ornithine transporter 1, in mutated-ER cells. This important observation shed new light on the metabolic adaptation of cancer cells to unique environments such as the liver. In 2024, I joined the lab of Dr. Gina DeNicola at Moffitt Cancer Center as a postdoctoral fellow in the Department of Physiology and Metabolism. I am currently studying the metabolic adaptations by which NRF2 hyperactivation drives non-small cell lung cancer metastasis, particularly through cystine/cysteine metabolism in both the circulation and during organ colonization, with a focus on brain and liver metastasis.