S Xia

Summary

Affiliation: Kennedy Krieger Institute
Country: USA

Publications

  1. ncbi Hepatocyte growth factor enhances death receptor-induced apoptosis by up-regulating DR5
    Yang Li
    Hugo W, Moser Research Institute at Kennedy Krieger, Baltimore, MD, USA
    BMC Cancer 8:325. 2008
  2. ncbi Regulation of glioblastoma stem cells by retinoic acid: role for Notch pathway inhibition
    M Ying
    Department of Neuro Oncology, Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA
    Oncogene 30:3454-67. 2011
  3. ncbi EphB2 receptor controls proliferation/migration dichotomy of glioblastoma by interacting with focal adhesion kinase
    S D Wang
    Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, MD, USA
    Oncogene 31:5132-43. 2012

Collaborators

  • S Wang
  • M Ying
  • Yang Li
  • A Quinones-Hinojosa
  • J Laterra
  • Y Sang
  • P Sun
  • C R Goodwin
  • H Guerrero-Cazares
  • B Lal
  • John Laterra
  • C Rory Goodwin
  • Xing Fan

Detail Information

Publications3

  1. ncbi Hepatocyte growth factor enhances death receptor-induced apoptosis by up-regulating DR5
    Yang Li
    Hugo W, Moser Research Institute at Kennedy Krieger, Baltimore, MD, USA
    BMC Cancer 8:325. 2008
    ..Dependent on cell context and the involvement of specific downstream effectors, both pro- and anti-apoptotic effects of HGF have been reported...
  2. ncbi Regulation of glioblastoma stem cells by retinoic acid: role for Notch pathway inhibition
    M Ying
    Department of Neuro Oncology, Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA
    Oncogene 30:3454-67. 2011
    ..Our findings identify mechanisms by which RA targets GBM-derived stem-like tumor-initiating cells and novel targets applicable to differentiation therapies for glioblastoma...
  3. ncbi EphB2 receptor controls proliferation/migration dichotomy of glioblastoma by interacting with focal adhesion kinase
    S D Wang
    Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, MD, USA
    Oncogene 31:5132-43. 2012
    ..These novel findings suggest that tumor cell invasion can be therapeutically targeted by inhibiting EphB2 signaling, and that optimal antitumor responses to EphB2 targeting may require concurrent use of anti-proliferative agents...