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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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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