Yunqing Li, Ph.D.

Yunqing Li
Yunqing Li
Research Scientist, Kennedy Krieger Institute

Kennedy Krieger Institute
707 N. Broadway
Baltimore, MD 21215
Phone: (443) 923-9526

Dr. Yunqing Li is a research scientist at the Hugo W. Moser Research Institute at Kennedy Krieger. She is also an assistant professor in the Department of Neurology at the Johns Hopkins University School of Medicine

Biographical Sketch:

Dr. Li pursued her undergraduate and graduate education at the Yunnan University in China. She then held a teaching position at the Kunming Medical College in China before pursuing her doctoral degree in medical genetics from Sichuan University. She came to the United States in 2003 to complete postdoctoral fellowships in the Department of Interdisciplinary Oncology at the H. Lee Moffitt Cancer Center and in the Department of Neurology at Kennedy Krieger Institute. In 2005, she was recruited as a faculty member for the Department of Neurology at the University of Virginia. In 2009, she joined the Kennedy Krieger Institute as a faculty member.

Dr. Li is a member of the American Association for Cancer Research. In 2001, she won a Natural Science Fund for Distinguished Young Scholars in Yunnan, China. In 2005, she was awarded a research fellowship by the American Brain Tumor Association. In 2011, she was awarded a discovery grant.

Research Summary:

Glioblastoma (GBM) is a very aggressive and fatal brain tumor. Despite aggressive therapy, the average median survival of patients with glioblastoma is approximately 15 months. Recently, subpopulations of tumor cells with stem cell-like properties have been identified in glioblastoma. These cells, typically referred to as glioma stem-like cells (GBM SCs) or glioma-initiating cells, are considered to be responsible for the propagation, recurrence, and therapeutic resistance of glioma. Dr. Li’s research focuses on understanding the origin of GBM SCs and the molecular mechanisms orchestrating GBM SCs maintenance. Her research studies the signaling pathways and transcriptional events that mediate GBM SCs growth. The goal of research is to develop new therapeutic strategies based on GBM SC targets. The techniques used are a wide array of state-of-the-art cancer research methods including molecular and cell biology, biochemistry, gene differential expression, gene knock-down and delivery techniques and animal studies.

Research Publications

Rath P, Lal B, Ajala O, Li Y, Xia S, Kim J, Laterra J. (2013). In Vivo c-Met Pathway Inhibition Depletes Human Glioma Xenografts of Tumor-Propagating Stem-Like Cells. Translational Oncology, 6(2),104-111.

Li Y, Laterra J. (2012). Cancer Stem Cells: Distinct Entities or Dynamically Regulated. Cancer Research, 72(3), 576-580.

Wang SD, Rath P, Lal B, Richard JP, Li Y, Goodwin CR, Laterra J, Xia S. (2012). EphB2 receptor controls proliferation/migration dichotomy of glioblastoma by interacting with focal adhesion kinase. Oncogene, 31(50), 5132-5143.

Li Y, Li A, Glas M, Lal B, Ying M, Sang Y, Xia S, Trageser D, Guerrero-Cázares H, Eberhart CG, Quiñones-Hinojosa A, Scheffler B, Laterra J. (2011). C-Met Signaling Induces a Reprogramming Network and Supports the Glioblastoma Stem-Like Phenotype. Proceedings of the National Academy of Sciences of the United States of America, 108(24), 9951-9956.

Ying M, Sang Y, Li Y, Guerrero-Cazares H, Quinones-Hinojosa A, Vescovi AL, Eberhart CG, Xia S, Laterra J. (2010). Krüppel-like family of transcription factor 9, a differentiation-associated transcription factor, suppresses Notch1 signaling and inhibits glioblastoma-initiating stem cells. Stem Cells, 29(1), 20-31.

Li Y, Guessous F, Zhang Y, DiPierro C, Kefas B, Johnson E, Marcinkiewicz L, Jiang J, Yang Y, Schmittgen TD, Lopes B, Schiff D, Purow B, Abounader R. (2009). MicroRNA-34a Inhibits Glioblastoma Growth by Targeting Multiple Oncogenes. Cancer Research, 69(19), 7569-7576.

Li Y, Guessous F, Kwon S, Kumar M, Ibidapo O, Fuller L, Johnson E, Lal B, Hussaini I, Bao Y, Laterra J, Schiff D, Abounader R. (2008). PTEN has tumor promoting properties in the setting of gain-of-function p53 mutations. Cancer Research, 68(6), 1723-1731.