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pubmed-article:2738645pubmed:abstractTextHuman glioblastomas are highly malignant intracranial tumors, some of which demonstrate amplification of the epidermal growth factor-receptor (EGF-R) gene. Overexpression of this gene is seen in the majority of primary tumors; however, the role of the EGF-R gene in glial tumorigenesis is unknown. The authors explored the relationship between EGF-R gene expression and glioblastoma cell growth in vitro and in vivo and found that this level of EGF-R gene expression did not correlate with tumor cell growth either in soft agar or in the nude mouse. This suggests that the EGF-R gene is not involved in effecting direct growth stimulation in glial oncogenesis. Tumorigenesis involves differentiation arrest; therefore, the expression of several proto-oncogenes in neuroectodermal tumors was investigated to evaluate the potential involvement of the EGF-R gene in glial differentiation. A nonoverlapping expression of the N-myc and EGF-R genes was found in neuronal-derived and glial-derived tumors, respectively. This suggests that the EGF-R gene may be involved in differentiation or its arrest in glia.lld:pubmed
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pubmed-article:2738645pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:2738645pubmed:articleTitleProto-oncogene abnormalities and their relationship to tumorigenicity in some human glioblastomas.lld:pubmed
pubmed-article:2738645pubmed:affiliationDivision of Neurological Surgery, University of California, San Diego.lld:pubmed
pubmed-article:2738645pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2738645pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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