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[Cancer Research 51, 2164-2172, April 15, 1991]
© 1991 American Association for Cancer Research
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Genes for Epidermal Growth Factor Receptor, Transforming Growth Factor {alpha}, and Epidermal Growth Factor and Their Expression in Human Gliomas in Vivo

A. Jonas Ekstrand, C. David James, Webster K. Cavenee, Barbara Seliger, Ralf F. Pettersson and V. Peter Collins1

Ludwig Institute for Cancer Research, Stockholm Branch, Box 60004, S-104 01 Stockholm, Sweden [A. J. E., B. S., R. F. P., V. P. C.]; Department of Neurosurgery, Henry Ford Hospital, Detroit, Michigan 48202 [C. D. J.]; Ludwig Institute for Cancer Research, Montreal Branch, Montreal, Canada [W. K. C.]; and Department of Pathology, Karolinska Hospital, Stockholm, Sweden [V. P. C.]

Anomalies of the epidermal growth factor receptor (EGFR) gene, including amplification, rearrangement, and overexpression, have been reported in malignant human gliomas in vivo. In vitro glioma cell lines coexpress EGFR and at least one of its ligands, transforming growth factor {alpha}, suggesting the existence of an autocrine growth stimulatory loop. We have studied the tumor tissue from 62 human glioma patients and examined the structure and quantity of the EGFR gene and its transcripts, as well as the quantity of the receptor protein. In addition we have examined the genes and transcripts coding for the pre-pro forms of epidermal growth factor and transforming growth factor {alpha}, the two endogenous EGFR ligands. EGFR gene amplification was detected in 16 of the 32 malignancy grade IV gliomas (glioblastoma) studied (50%), but only in 1 of 30 gliomas of lesser malignancy grade (I–III). All tumors with an amplified gene overexpressed EGFR mRNA. More than one-half (62.5%) of the glioblastomas with amplified EGFR genes also showed coamplification of rearranged EGFR genes and concomitant expression of aberrant mRNA species. Overexpression, without gene amplification, was observed in some of the low grade gliomas, and aberrant EGFR transcripts were also seen in some cases without gene amplification or detected gene rearrangements. mRNA expression for one or both of the pre-pro forms of the ligands was detected in every tumor studied. Thus, several mechanisms for the activation of the EGFR-mediated growth stimulating pathway are possible in human gliomas in vivo: expression of a structurally altered receptor that may have escaped normal control mechanisms; and/or auto-, juxta-, or paracrine stimulating mechanisms involving coexpression of receptor and ligands, with or without overexpression of the receptor.

1 To whom requests for reprints should be addressed, at Ludwig Institute for Cancer Research, Box 60004, S-104 01 Stockholm, Sweden.

Received 10/16/90. Accepted 2/ 7/91.




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Copyright © 1991 by the American Association for Cancer Research.