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Genetic Determinants of Neoplastic Transformation by the Retroviral Oncogene v-erbB
Alan Wells and J. Michael Bishop
Proceedings of the National Academy of Sciences of the United States of America
Vol. 85, No. 20 (Oct. 15, 1988), pp. 7597-7601
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/32991
Page Count: 5
You can always find the topics here!Topics: Alleles, 3T3 cells, Erythroid cells, Cells, Tumors, Oncogenes, NIH 3T3 cells, Chimeras, Cell culture techniques, Cell growth
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The retroviral oncogene v-erbB is a mutant version of the gene (c-erbB or ERBB1) that encodes the cell-surface epidermal growth factor receptor (EGFR). The mutations take three forms: (i) a large deletion that removes the entire ligand-binding domain of EGFR, (ii) smaller deletions that affect the carboxyl-terminal domain of EGFR, and (iii) point mutations that cause conservative substitutions of amino acids. Previous work has shown that, in the absence of the large deletion, ERBB1 cannot transform cells autonomously. Here we report that when the large deletion is present, no other mutation is required for ERBB1 to transform established rodent fibroblasts to a tumorigenic phenotype. In particular, there is no need for deletions affecting the carboxyl terminus of the gene product. It appears, therefore, that removal of the ligand-binding domain from the EGFR suffices to create a transforming protein. Deletions at the carboxyl terminus of the EGFR apparently play only a secondary role in transformation by affecting the host range and perhaps the potency of transformation; and there is as yet no evidence to implicate point mutations in the activation of ERBB1 to an oncogene. Our findings support the view that augmented activity of the EGFR can contribute to tumorigenesis.
Proceedings of the National Academy of Sciences of the United States of America © 1988 National Academy of Sciences