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Overexpression of c-MYC promotes an undifferentiated phenotype in cultured astrocytes and allows elevated Ras and Akt signaling to induce gliomas from GFAP-expressing cells in mice

Published online by Cambridge University Press:  25 October 2004

ANDREW B. LASSMAN
Affiliation:
Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, NY
CHENGKAI DAI
Affiliation:
Current address: Whitehead Institute, Massachusetts Institute of Technology, Boston, MA Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY
GREGORY N. FULLER
Affiliation:
Department of Pathology, MD Anderson Cancer Center, Houston, TX
ANDREW J. VICKERS
Affiliation:
Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY
ERIC C. HOLLAND
Affiliation:
Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, NY Department of Surgery (Neurosurgery), Memorial Sloan-Kettering Cancer Center, New York, NY Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY

Abstract

The c-MYC protooncogene is overexpressed in the most malignant primary brain tumor, glioblastoma multiforme (GBM), and has been correlated with the undifferentiated character of several cell types. However, the role of Myc activity in the generation of GBMs is not known. In this report, we show that gene transfer of c-MYC to GFAP-expressing astrocytes in vitro promotes the outgrowth of GFAP-negative, nestin-expressing cells with progenitor-like morphology, growth characteristics and gene-expression pattern. In addition, gene transfer of c-MYC to GFAP-expressing astrocytes in vivo induces GBMs when co-expressed with activated Ras and Akt. Without c-MYC, Ras+Akt induces GBMs from nestin-expressing CNS progenitors but is insufficient in GFAP-expressing differentiated astrocytes. The ability of Myc activity to enhance the oncogenic effects of Ras+Akt appears to be limited to GFAP-expressing astrocytes because nestin-expressing progenitors show no increase in GBM formation with the addition of MYC to Ras+Akt. These studies indicate that one role of MYC activity in the formation of gliomas might be to either promote or reinforce an undifferentiated phenotype required for glioma cells to respond to the oncogenic effects of elevated Ras and Akt activity.

Type
Research Article
Copyright
© Cambridge University Press 2004

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Overexpression of c-MYC promotes an undifferentiated phenotype in cultured astrocytes and allows elevated Ras and Akt signaling to induce gliomas from GFAP-expressing cells in mice
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Overexpression of c-MYC promotes an undifferentiated phenotype in cultured astrocytes and allows elevated Ras and Akt signaling to induce gliomas from GFAP-expressing cells in mice
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