Skip Navigation

JNCI Journal of the National Cancer Institute 1989 81(1):63-67; doi:10.1093/jnci/81.1.63
© 1989 by Oxford University Press
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Gerosa, M. A.
Right arrow Articles by valle, G. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gerosa, M. A.
Right arrow Articles by valle, G. D.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 81, No. 1, 63-67, January 1989
© 1989 Oxford University Press

Overexpression of N-ras Oncogene and Epidermal Growth Factor Receptor Gene in Human Glioblastomas

Massimo A. Gerosa, Daniela Talarico, Caterina Fognani, Elena Raimondi, Marco Colombatti, Giuseppe Tridente, Luigi De Carli, Giuliano Della valle

Departments of Neurosurgery, University of Verona Verona, Italy
Departments of Immunology, University of Verona Verona, Italy
Departments of Genetics and Microbiology "A. Buzzati-Traverso," University of Pavia Pavia, Italy
Department of Animal Biology, University of Catania Catania, Italy

Correspondence to: Dr. Massimo A. Gerosa, Dept. of Neurosurgery, Ospedale Geriatrico, Via Mameli, 37100 Verona, Italy.

Present address: D. Talarico, Department of Pathology, New York University Medical Center, New York, NY. G. Della Valle, Department of Animal Biology, University of Catania, Catania, Italy.

Five human glioblastoma cell lines were analyzed for oncogene activation with a panel of probes. Abnormal expression of the epidermal growth factor receptor (EGFr) gene was detected in four of five lines; N-ras oncogene overexpression was found in all five cell lines. These results were subsequently confirmed with fresh brain tumor and nonneoplastic brain tissue biopsy samples; increased expression of the N-ras proto-oncogene was observed in five of five glioblastomas, all of which also showed EGFr gene overex-pression, but not in well-differentiated gliomas or in nonneoplastic brain tis-sue specimens. No significant differ-ences in Ha-ras and Ki-ras expression were observed. Preliminary histochem-ical observations showed that intra-cellular levels of transforming growth factor {alpha}, a putative biochemical link between these two oncogenes, were significantly higher in glioblastoma cells than in controls. [J Natl Cancer Inst 1989;81:63–67]



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Neuro Oncol DukeHome page
B. Kaur, F. W. Khwaja, E. A. Severson, S. L. Matheny, D. J. Brat, and E. G. Van Meir
Hypoxia and the hypoxia-inducible-factor pathway in glioma growth and angiogenesis
Neuro-oncol, April 1, 2005; 7(2): 134 - 153.
[Abstract] [PDF]


Home page
Neuro Oncol DukeHome page
T. L. Glass, T.-J. Liu, and W.K. A. Yung
Inhibition of cell growth in human glioblastoma cell lines by farnesyltransferase inhibitor SCH66336
Neuro-oncol, July 1, 2000; 2(3): 151 - 158.
[Abstract] [PDF]


Home page
Mol. Biol. CellHome page
S. K. Kuwada and X. Li
Integrin alpha 5/beta 1 Mediates Fibronectin-dependent Epithelial Cell Proliferation through Epidermal Growth Factor Receptor Activation
Mol. Biol. Cell, July 1, 2000; 11(7): 2485 - 2496.
[Abstract] [Full Text]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.