Abstract
Epidermal growth factor (EGF), through interaction with specific cell surface receptors, generates a pleiotropic response that, by a poorly defined mechanism, can induce proliferation of target cells1–4. Subversion of the EGF mitogenic signal through expression of a truncated receptor5–7 may be involved in transformation by the avian erythroblastosis virus (AEV) oncogene v-erb-B, suggesting that similar EGF receptor defects may be found in human neoplasias. Overexpression of EGF receptors has been reported on the epidermoid carcinoma cell line A431 (ref. 8), in various primary brain tumours9 and in squamous carcinomas10. In A431 cells the receptor gene is amplified6,11,12. Here we show that 4 of 10 primary brain tumours of glial origin which express levels of EGF receptors that are higher than normal also have amplified EGF receptor genes. Amplified receptor genes were not detected in the other brain tumours examined. Further analysis of EGF receptor defects may show that such altered expression and amplification is a particular feature of certain human tumours.
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References
Cohen, S. J. biol. Chem. 237, 1555–1562 (1962).
Schlessinger, J. et al. Membranes in Growth and Development 359–372 (Liss, New York, 1982).
Carpenter, G. & Cohen, S. A. Rev. Biochem. 48, 193–216 (1979).
Schlessinger, J. et al. CRC crit. Rev. Biochem. 14, 93–111 (1983).
Downward, J. et al. Nature 307, 521–527 (1984).
Ullrich, A. et al. Nature 309, 418–425 (1984).
Yamamoto, et al. Cell 35, 71–78 (1983).
Fabricant, R. N., DcLarco, J. E. & Todaro, G. J. Proc. natn. Acad. Sci. U.S.A. 74, 565–569 (1977).
Libermann, T. A. et al. Cancer Res. 44, 753–760 (1984).
Cowley, G., Smith, J. A., Gusterson, B., Hendler, F. & Ozanne, B. in Cancer Cells I (eds Levine, A. J. et al.) 5–10 (Cold Spring Harbor Laboratory, New York, 1984).
Merlino, G. T. et al. Science 224, 417–419 (1984).
Lin, C. R. et al. Science 224, 843–848 (1984).
Xu, Y.-H. et al. Nature 309, 806–810 (1984).
Schimke, R. J. Cell 37, 705–715 (1984).
Mayes, E. L. V. & Waterfield, M. D. EMBO J 3, 531–537 (1984).
Weber, W., Gill, G. N. & Spiess, J. Science 224, 294–297 (1984).
Dalla-Favera, R., Wong-Staal, F. & Gallo, R. C. Nature 299, 61–63 (1982).
Kohl, N. E. et al. Cell 35, 359–367 (1983).
Schwazb, M. et al. Nature 305, 245–248 (1983).
Schwab, M. K. et al. Proc. natn. Acad. Sci. U.S.A. 81, 4940–4944 (1984).
Hayashi, K., Kakizoe, T. & Sugimura, T. Gann 74, 798–901 (1983).
Collins, S. & Groudine, M. Nature 298, 679–681 (1982).
Shimizu, N., Behzsdian, M. A. & Shimizu, Y. Proc. natn. Acad. Sci. U.S.A. 77, 3600 (1980).
Davies, R. L., Grosse, V. A., Kucherlapati, R. & Bothwell, M. Proc. natn. Acad. Sci. U.S.A. 77, 4188–4192 (1980).
Shapiro, J. R., Yung, W.-K. A. & Shapiro, W. R. Cancer Res. 41, 2349–2359 (1981).
Bartal, A. D., Heilbronn, Y. D. & Schiffer, J. Surg. Neurol. 1, 337–342 (1973).
Mark, J., Westermark, B., Ponten, J. & Hugosson, R. Hereditas 87, 243–260 (1977).
Maniatis, T., Fritsch, E. F. & Sambrook, J. Molecular Cloning (Cold Spring Harbor Laboratory, New York, 1982).
Helfman, D. M., Feramisco, J. R., Fiddes, J. C., Thomas, G. P. & Hughes, S. H. Proc. natn. Acad. Sci. U.S.A. 8, 31–35 (1983).
Maxam, A. M. & Gilbert, W. Meth. Enzym. 65, 499–560 (1980).
Taylor, J. M., Illmensee, R. & Summers, J. Biochim. biophys. Acta 4, 324–330 (1976).
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Libermann, T., Nusbaum, H., Razon, N. et al. Amplification, enhanced expression and possible rearrangement of EGF receptor gene in primary human brain tumours of glial origin. Nature 313, 144–147 (1985). https://doi.org/10.1038/313144a0
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DOI: https://doi.org/10.1038/313144a0
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