Wen-Shu Wu, PhD

Associate Professor

College of Medicine


Cancer Biology

Full Member

Phone: 312-996-2586

Email: wuwenshu@uic.edu

My early research training at the Ph.D. level inspired a passion for molecular mechanisms regulating hematopoiesis and hematopoietic stem/progenitor cells. To further my experimental skills and strategies, I performed a postdoctoral fellowship in the laboratory of Dr. Thomas Look at Dana-Farber Cancer Institute/ Harvard Medical School, who was an expert in hematopoiesis and leukemogenesis.Since establishing my independent research laboratory in 2006, I have utilized this experience to successfully run my own successful research program in stem cell biology. I have a broad interest in stem cell biology. We pioneered 4-in-1 reprogramming vectors for efficient generation of fully reprogrammed induced pluripotent stem (iPS) cells from somatic cells. Recently, we developed a novel system for knockdown of gene expression, named as transcription activator-like effector (TALE)- based transcriptional repressor. Using this system, we knocked down expression of miR-302/367 cluster in human iPS and ES cells.The current proposal was developed based on my long-term interests in the area of hematopoiesis and leukemia. We have been studying the role of Slug/Snail2 in hematopoiesis and self-renewal of normal hematopoietic stem cells (HSCs) under static and stress conditions. We found that Slug/Snail2 is dispensable for the maintenance of HSCs under normal physiological conditions but essential for the survival of HSCs after injured by irradiation.Moreover, Slug/Snail2 ablation enhances the self-renewal of HSCs during hematopoietic regeneration. In this proposal, our preliminary studies showed that deletion of Slug/Snail2 impairs pathogenesis of MLL-AF9-induced acute myeloid leukemia (AML) and results in a loss of leukemia stem cells (LSCs). In the proposed studies in this project, we will delineate cellular and molecular mechanisms whereby Slug/Snail2 impacts the development and progression of MLL-AF9-induced AMLs through a set of key downstream targets in LSCs. We will also test therapeutic effects of targeting Slug/Snial2 and its downstream targets.Successful completion of this will advance our understating on pathogenesis of MLL-rearranged AMLs and provide a rationale for targeting Slug/Snail2 or its critical downstream targets in LSCs as novel therapeutic approaches for treating this presently therapy-resistant disease. Considering role of Slug/Snail2 in normal HSCs, we predict that targeting Slug/Snail2 will unlikely have negative effects on the maintenance an

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