Ets Factors Regulate Neural Stem Cell Depletion and Gliogenesis in Ras Pathway Glioma. Breunig, J. J., Levy, R., Antonuk, C. D., Molina, J., Dutra-Clarke, M., Park, H., Akhtar, A. A., Kim, G. B., Hu, X., Bannykh, S. I., Verhaak, R. G., & Danielpour, M. Cell Rep, 12(2):258-71, 2015. 2211-1247 Breunig, Joshua J Levy, Rachelle Antonuk, C Danielle Molina, Jessica Dutra-Clarke, Marina Park, Hannah Akhtar, Aslam Abbasi Kim, Gi Bum Hu, Xin Bannykh, Serguei I Verhaak, Roel G W Danielpour, Moise P30 CA016672/CA/NCI NIH HHS/United States Journal Article Research Support, Non-U.S. Gov't United States 2015/07/07 Cell Rep. 2015 Jul 14;12(2):258-71. doi: 10.1016/j.celrep.2015.06.012. Epub 2015 Jul 2.
doi  abstract   bibtex   
As the list of putative driver mutations in glioma grows, we are just beginning to elucidate the effects of dysregulated developmental signaling pathways on the transformation of neural cells. We have employed a postnatal, mosaic, autochthonous glioma model that captures the first hours and days of gliomagenesis in more resolution than conventional genetically engineered mouse models of cancer. We provide evidence that disruption of the Nf1-Ras pathway in the ventricular zone at multiple signaling nodes uniformly results in rapid neural stem cell depletion, progenitor hyperproliferation, and gliogenic lineage restriction. Abolishing Ets subfamily activity, which is upregulated downstream of Ras, rescues these phenotypes and blocks glioma initiation. Thus, the Nf1-Ras-Ets axis might be one of the select molecular pathways that are perturbed for initiation and maintenance in glioma.
@article{RN6141,
   author = {Breunig, J. J. and Levy, R. and Antonuk, C. D. and Molina, J. and Dutra-Clarke, M. and Park, H. and Akhtar, A. A. and Kim, G. B. and Hu, X. and Bannykh, S. I. and Verhaak, R. G. and Danielpour, M.},
   title = {Ets Factors Regulate Neural Stem Cell Depletion and Gliogenesis in Ras Pathway Glioma},
   journal = {Cell Rep},
   volume = {12},
   number = {2},
   pages = {258-71},
   note = {2211-1247
Breunig, Joshua J
Levy, Rachelle
Antonuk, C Danielle
Molina, Jessica
Dutra-Clarke, Marina
Park, Hannah
Akhtar, Aslam Abbasi
Kim, Gi Bum
Hu, Xin
Bannykh, Serguei I
Verhaak, Roel G W
Danielpour, Moise
P30 CA016672/CA/NCI NIH HHS/United States
Journal Article
Research Support, Non-U.S. Gov't
United States
2015/07/07
Cell Rep. 2015 Jul 14;12(2):258-71. doi: 10.1016/j.celrep.2015.06.012. Epub 2015 Jul 2.},
   abstract = {As the list of putative driver mutations in glioma grows, we are just beginning to elucidate the effects of dysregulated developmental signaling pathways on the transformation of neural cells. We have employed a postnatal, mosaic, autochthonous glioma model that captures the first hours and days of gliomagenesis in more resolution than conventional genetically engineered mouse models of cancer. We provide evidence that disruption of the Nf1-Ras pathway in the ventricular zone at multiple signaling nodes uniformly results in rapid neural stem cell depletion, progenitor hyperproliferation, and gliogenic lineage restriction. Abolishing Ets subfamily activity, which is upregulated downstream of Ras, rescues these phenotypes and blocks glioma initiation. Thus, the Nf1-Ras-Ets axis might be one of the select molecular pathways that are perturbed for initiation and maintenance in glioma.},
   keywords = {Animals
Brain/metabolism/pathology
Brain Neoplasms/metabolism/*pathology
DNA-Binding Proteins/metabolism
Genes, Reporter
Glioma/metabolism/*pathology
Immunohistochemistry
Mice
Microscopy, Confocal
Neural Stem Cells/cytology/metabolism
Neurofibromin 1/antagonists & inhibitors/genetics/metabolism
Proto-Oncogene Proteins c-ets/genetics/*metabolism
RNA Interference
RNA, Small Interfering/metabolism
Signal Transduction
Transcription Factors/metabolism
Up-Regulation
ras Proteins/*metabolism},
   DOI = {10.1016/j.celrep.2015.06.012},
   year = {2015},
   type = {Journal Article}
}

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