This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Reifenberger, G. Articles by Collins, V. P. Search for Related Content PubMed PubMed Citation Articles by Reifenberger, G. Articles by Collins, V. P.

American Journal of Pathology, Vol 147, 245-250, Copyright © 1995 by American Society for Investigative Pathology

REGULAR ARTICLES

Coexpression of transforming growth factor-alpha and epidermal growth factor receptor in capillary hemangioblastomas of the central nervous system

G Reifenberger, J Reifenberger, T Bilzer, W Wechsler and VP Collins
Department of Neuropathology, Heinrich-Heine-University, Dusseldorf, Germany.

The expression of epidermal growth factor receptor (EGFR) and the pre- pro form of one of its ligands, transforming growth factor-alpha (TGF- alpha), was studied by Northern blotting in a series of 14 capillary hemangioblastomas of the central nervous system. A constant coexpression of EGFR and pre-pro-TGF-alpha mRNAs was found. Immunocytochemical investigation of an extended series of 51 capillary hemangioblastomas revealed that the stromal cells in these tumors showed immunoreactivity with monoclonal antibodies to EGFR and TGF- alpha. Analysis of gene dosage by Southern blotting in 20 tumors indicated a normal gene copy number of EGFR and TGF alpha in all cases. Our findings suggest that autocrine and/or juxtacrine growth stimulation via the EGFR may contribute to tumor growth in capillary hemangioblastomas.

This article has been cited by other articles:

				S. Glasker, J. Li, J. B. Xia, H. Okamoto, W. Zeng, R. R. Lonser, Z. Zhuang, E. H. Oldfield, and A. O. Vortmeyer Hemangioblastomas share protein expression with embryonal hemangioblast progenitor cell. Cancer Res., April 15, 2006; 66(8): 4167 - 4172. [Abstract] [Full Text] [PDF]

				J. An and M. B. Rettig Mechanism of von Hippel-Lindau Protein-Mediated Suppression of Nuclear Factor kappa B Activity Mol. Cell. Biol., September 1, 2005; 25(17): 7546 - 7556. [Abstract] [Full Text] [PDF]

				W. Y. Kim and W. G. Kaelin Role of VHL Gene Mutation in Human Cancer J. Clin. Oncol., December 15, 2004; 22(24): 4991 - 5004. [Abstract] [Full Text] [PDF]

				L. Gunaratnam, M. Morley, A. Franovic, N. de Paulsen, K. Mekhail, D. A. E. Parolin, E. Nakamura, I. A. J. Lorimer, and S. Lee Hypoxia Inducible Factor Activates the Transforming Growth Factor-{alpha}/Epidermal Growth Factor Receptor Growth Stimulatory Pathway in VHL-/- Renal Cell Carcinoma Cells J. Biol. Chem., November 7, 2003; 278(45): 44966 - 44974. [Abstract] [Full Text] [PDF]

				H. Yang and W. G. Kaelin Jr. Molecular Pathogenesis of the Von Hippel-Lindau Hereditary Cancer Syndrome: Implications for Oxygen Sensing Cell Growth Differ., September 1, 2001; 12(9): 447 - 455. [Full Text] [PDF]

				M. A. Hoffman, M. Ohh, H. Yang, J. M. Klco, M. Ivan, and W. G. Kaelin Jr von Hippel-Lindau protein mutants linked to type 2C VHL disease preserve the ability to downregulate HIF Hum. Mol. Genet., May 1, 2001; 10(10): 1019 - 1027. [Abstract] [Full Text] [PDF]