Biography: While a medical student in Russia, my research was focused on various aspects of clinical and molecular microbiology. After graduating from medical school, I pursued a Ph.D. in biochemistry and my research under the mentorship of Dr. G. Douglas Markham at the Fox Chase Cancer Center in Philadelphia was focused on the role of the metabolic enzyme IMP dehydrogenase in the regulation of purine and energy metabolism. Subsequently, my interest in pediatric hematology/oncology and blood development prompted me to join the laboratory of Dr. Mitchell Weiss at the Children’s Hospital of Philadelphia, where I studied the global transcriptional networks that govern hematopoietic lineage priming and specification. In 2011 I joined a Pediatric Residency program at the Children’s Hospital of Pittsburgh, which I finished in 2014, followed by fellowship training in Pediatric Hematology Oncology at the Boston Children’s/Dana-Farber Cancer and Blood Disorders Center from 2014-2017. I am looking forward to a productive academic career where I hope to combine clinical work with basic research in hematopoiesis, stem cell biology and cancer, with the ultimate goal of establishing an independent, NIH-funded laboratory.
Lay Description: MLL-rearranged acute myeloid leukemia (AML) is a subtype of pediatric AML with extremely poor prognosis. Our laboratory studies transcription factors - proteins that regulate the work of genes. In our prior study, we identified several transcription factors as strong selective dependencies in MLL-rearranged AML, i.e. depletion of these two proteins is selectively toxic to a specific type of leukemia cells. Importantly, our preliminary data indicates that inhibition of these proteins does not impair normal blood development. This suggests a potential “Achilles heel” for leukemia-specific therapy with little or no toxic effects on normal tissues. We propose to study why MLL-rearranged AML is so "addicted" to these proteins. We will use a combination of genetic, biochemical and systems biology approaches. In addition, we propose to use a cutting-edge engineered chemical degradation system to evaluate the therapeutic potential of inhibiting these transcription factors in a mouse model of human AML. Our study will validate and mechanistically characterize transcriptional addiction as a potential therapeutic strategy in pediatric AML.
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