Abstract
Cell surface receptors have been traditionally defined through their specific interaction with purified ligands, but the study of oncogene-coded tyrosine kinases and their proto-oncogene homologs has presented the reciprocal problem — namely, can ligands for putative receptors be identified? The demonstration that the v-erbB oncogene encodes a truncated form of the epidermal growth factor (EGF) receptor (Downward et al. 1984b) provided the first direct evidence that certain oncogene products could be derived from receptor genes, and underscored the possibility that critical alterations in receptor function might directly contribute to neoplasia. Investigators now suspect that other retroviral oncogenes of the tyrosine kinase gene family (v-src, v-abl, v-fes/fps, v-yes, v-fgr, and v-ros), as well as functionally related oncogenes derived from tumor cells (neu, trk, met), could also have arisen from receptor genes. One paradigm involves a member of this gene family, c-fms, which encodes a product related, and possibly identical, to the receptor for the macrophage colony-stimulating factor, CSF-1 (Sherr et al. 1985).
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Sherr, C.J., Stanley, E.R. (1986). The c-fms Proto-Oncogene and the CSF-1 Receptor. In: Kahn, P., Graf, T. (eds) Oncogenes and Growth Control. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73325-3_13
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DOI: https://doi.org/10.1007/978-3-642-73325-3_13
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