Deletion-mutant epidermal growth factor receptor in human gliomas: Effect of type II mutation on receptor function

Peter A. Humphrey; Lisa M. Gangarosa; Albert J. Wong; Gerald E. Archer; Morten Lund-Johansen; Rolf Bjerkvig; Ole Didrik Laerum; Henry S. Friedman; Darell D. Bigner

doi:10.1016/0006-291X(91)91051-D

Deletion-mutant epidermal growth factor receptor in human gliomas: Effect of type II mutation on receptor function

Peter A. Humphrey^*
, Lisa M. Gangarosa
, Albert J. Wong
, Gerald E. Archer
, Morten Lund-Johansen
, Rolf Bjerkvig
, Ole Didrik Laerum
, Henry S. Friedman
, Darell D. Bigner

^*Corresponding author for this work

Research output: Contribution to journal › Article › Research › peer-review

91 Citations (Scopus)

Abstract

Malignant human glioma D-298 MG amplifies a rearranged epidermal growth factor receptor (EGFR) gene (c-erbB proto-oncogene), resulting in an in-frame deletion of 83 amino acids in domain IV of the extracellular domain of the EGFR. EGF and transforming growth factor-α (TGF-α) bound to the mutant EGFR with high affinity and enhanced the intrinsic mutant EGFR kinase activity. The mutant EGFR was capable of transducing EGF-stimulated glioma cell proliferation and invasiveness in an in vitro three-dimensional spheroid model. The deletion-mutant EGFR in D-298 MG is capable of being activated by growth factor; this suggests that overexpression of this mutant EGFR protein rather than structural alteration may be the more significant biologic event.

Original language	English
Pages (from-to)	1413-1420
Number of pages	8
Journal	Biochemical and Biophysical Research Communications
Volume	178
Issue number	3
DOIs	https://doi.org/10.1016/0006-291X(91)91051-D
Publication status	Published - 15 Aug 1991
Externally published	Yes

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10.1016/0006-291X(91)91051-D

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Humphrey, P. A., Gangarosa, L. M., Wong, A. J., Archer, G. E., Lund-Johansen, M., Bjerkvig, R., Laerum, O. D., Friedman, H. S., & Bigner, D. D. (1991). Deletion-mutant epidermal growth factor receptor in human gliomas: Effect of type II mutation on receptor function. Biochemical and Biophysical Research Communications, 178(3), 1413-1420. https://doi.org/10.1016/0006-291X(91)91051-D

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title = "Deletion-mutant epidermal growth factor receptor in human gliomas: Effect of type II mutation on receptor function",

abstract = "Malignant human glioma D-298 MG amplifies a rearranged epidermal growth factor receptor (EGFR) gene (c-erbB proto-oncogene), resulting in an in-frame deletion of 83 amino acids in domain IV of the extracellular domain of the EGFR. EGF and transforming growth factor-α (TGF-α) bound to the mutant EGFR with high affinity and enhanced the intrinsic mutant EGFR kinase activity. The mutant EGFR was capable of transducing EGF-stimulated glioma cell proliferation and invasiveness in an in vitro three-dimensional spheroid model. The deletion-mutant EGFR in D-298 MG is capable of being activated by growth factor; this suggests that overexpression of this mutant EGFR protein rather than structural alteration may be the more significant biologic event.",

author = "Humphrey, \{Peter A.\} and Gangarosa, \{Lisa M.\} and Wong, \{Albert J.\} and Archer, \{Gerald E.\} and Morten Lund-Johansen and Rolf Bjerkvig and Laerum, \{Ole Didrik\} and Friedman, \{Henry S.\} and Bigner, \{Darell D.\}",

note = "Funding Information: ACKNOWIXI\textasciitilde{}GMEN'I'S: We wish to thank Stella Cook and Paris Scott for expert technical assistance, Theresa Roberts for aid in preparing the manuscri t, Ann Tamariz for editorial assistance, and Susan Embry and Steve Conlon P or preparation of the photographs. This research was supported in part by grants from the McDonnell Foundation, the American Cancer Society (89-171) and the National Institutes of Health (NS20023-05, T32N507304, CA11898, and CA32672). L. M. G. was a Howard Hughes Medical Institute medical student research training fellow.",

year = "1991",

month = aug,

day = "15",

doi = "10.1016/0006-291X(91)91051-D",

language = "English",

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journal = "Biochemical and Biophysical Research Communications",

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Humphrey, PA, Gangarosa, LM, Wong, AJ, Archer, GE, Lund-Johansen, M, Bjerkvig, R, Laerum, OD, Friedman, HS & Bigner, DD 1991, 'Deletion-mutant epidermal growth factor receptor in human gliomas: Effect of type II mutation on receptor function', Biochemical and Biophysical Research Communications, vol. 178, no. 3, pp. 1413-1420. https://doi.org/10.1016/0006-291X(91)91051-D

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T1 - Deletion-mutant epidermal growth factor receptor in human gliomas

T2 - Effect of type II mutation on receptor function

AU - Humphrey, Peter A.

AU - Gangarosa, Lisa M.

AU - Wong, Albert J.

AU - Archer, Gerald E.

AU - Lund-Johansen, Morten

AU - Bjerkvig, Rolf

AU - Laerum, Ole Didrik

AU - Friedman, Henry S.

AU - Bigner, Darell D.

N1 - Funding Information: ACKNOWIXI~GMEN'I'S: We wish to thank Stella Cook and Paris Scott for expert technical assistance, Theresa Roberts for aid in preparing the manuscri t, Ann Tamariz for editorial assistance, and Susan Embry and Steve Conlon P or preparation of the photographs. This research was supported in part by grants from the McDonnell Foundation, the American Cancer Society (89-171) and the National Institutes of Health (NS20023-05, T32N507304, CA11898, and CA32672). L. M. G. was a Howard Hughes Medical Institute medical student research training fellow.

PY - 1991/8/15

Y1 - 1991/8/15

N2 - Malignant human glioma D-298 MG amplifies a rearranged epidermal growth factor receptor (EGFR) gene (c-erbB proto-oncogene), resulting in an in-frame deletion of 83 amino acids in domain IV of the extracellular domain of the EGFR. EGF and transforming growth factor-α (TGF-α) bound to the mutant EGFR with high affinity and enhanced the intrinsic mutant EGFR kinase activity. The mutant EGFR was capable of transducing EGF-stimulated glioma cell proliferation and invasiveness in an in vitro three-dimensional spheroid model. The deletion-mutant EGFR in D-298 MG is capable of being activated by growth factor; this suggests that overexpression of this mutant EGFR protein rather than structural alteration may be the more significant biologic event.

AB - Malignant human glioma D-298 MG amplifies a rearranged epidermal growth factor receptor (EGFR) gene (c-erbB proto-oncogene), resulting in an in-frame deletion of 83 amino acids in domain IV of the extracellular domain of the EGFR. EGF and transforming growth factor-α (TGF-α) bound to the mutant EGFR with high affinity and enhanced the intrinsic mutant EGFR kinase activity. The mutant EGFR was capable of transducing EGF-stimulated glioma cell proliferation and invasiveness in an in vitro three-dimensional spheroid model. The deletion-mutant EGFR in D-298 MG is capable of being activated by growth factor; this suggests that overexpression of this mutant EGFR protein rather than structural alteration may be the more significant biologic event.

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JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 3

ER -

Deletion-mutant epidermal growth factor receptor in human gliomas: Effect of type II mutation on receptor function

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