Affiliation: Kennedy Krieger Institute
- c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotypeYunqing Li
Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 108:9951-6. 2011..These findings show that c-Met enhances the population of glioblastoma stem cells (GBM SCs) via a mechanism requiring Nanog and potentially other c-Met-responsive reprogramming transcription factors...
- Cancer stem cells: distinct entities or dynamically regulated phenotypes?Yunqing Li
Hugo W Moser Research Institute at Kennedy Krieger, and Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
Cancer Res 72:576-80. 2012..Understanding the dynamic equilibrium between CSCs and cancer progenitor cells is critical for the development of therapeutic strategies to deplete tumors of their tumor-propagating and treatment-resistant cell subpopulations...
- Krüppel-like family of transcription factor 9, a differentiation-associated transcription factor, suppresses Notch1 signaling and inhibits glioblastoma-initiating stem cellsMingyao Ying
Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, Maryland 21205, USA
Stem Cells 29:20-31. 2011..Our results show for the first time that KLF9 has differentiating and tumor-suppressing functions in tumor-initiating stem cells...
- The scatter factor/hepatocyte growth factor: c-met pathway in human embryonal central nervous system tumor malignancyYunqing Li
Department of Neurology, Johns Hopkins University School of Medicine, MD 21205, USA
Cancer Res 65:9355-62. 2005..This first characterization establishes SF/HGF:c-Met as a new pathway of malignancy with multifunctional effects in human embryonal CNS tumors...