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Dr. Da-Qiang Li, M.D., now is a full professor of Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University. He received M.D. degree from Chongqing Medical University (Chongqing, China) in 2003, and then completed his postdoctoral training at Fudan University, Case Western Reserve University (Cleveland, OH), University of Texas M.D. Anderson Cancer Center (Houston, TX) and George Washington University (Washington, DC). In November 2009, he was appointed as a Faculty and an Assistant Research Professor at Department of Biochemistry and Molecular Medicine, George Washington University, and then promoted to an Associate Research Professor position in July, 2013 at the same institute. In September, 2013, he joined in Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University as a full professor and Principle Investigator. His research projects mainly focus on understanding the molecular mechanism of tumor invasion and metastasis and therapeutic resistance. To date, he has published over 50 SCI papers, including Cancer Cell, Mol Cell, Cell Rep,Hepatology, J Cell Biol, Nat Commun, PNAS, Autophagy, Nucleic Acids Res, Cancer Res, and Cell Death Differ. Currently he is an editorial board member for 6 international journals including Cancer Research.
Research Focus: Molecular mechanisms of tumor metastasis and therapeutic resistance Although advances have been made in tumor diagnosis and therapies, most cancer-related deaths still result from tumor invasion and metastasis. An appreciation of the molecular mechanisms to control the invasive and metastatic behavior of cancer cells may likewise lead to better methods to control their growth and spread within host tissues. Another leading cause of cancer-related death is increased chemo-resistance and radio-resistance of cancer cells. It is increasingly recognized the importance of DNA repair in cancer therapeutic resistance. Thus, my research projects primarily involve those two related areas, including understanding of the molecular mechanism of tumor invasion and metastasis and targeting DNA repair pathways to reduce cancer therapeutic resistance.
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