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Mechanisms involving an expanding erbB/EGF receptor family of tyrosine kinases in human neoplasia

  • Chapter
Genes, Oncogenes, and Hormones

Part of the book series: Cancer Treatment and Research ((CTAR,volume 61))

Abstract

Compelling evidence for the involvement in the neoplastic process of molecules regulating normal cellular growth originates from observations demonstrating that the transduced oncogenes of certain acute transforming retroviruses represent activated versions of growth factors or growth factor receptors. When incorporated within the retroviral genome, such transduced sequences acquire the ability to induce neoplastic transformation. Analysis of viral oncogene products has revealed important insights into the function of their normal cellular counterparts, designated protooncogenes. For example, in AEV-induced neoplasia, the EGF receptor gene (c-erbB) is activated as an oncogene (v-erbB) upon amino-terminal truncation of the coding sequence combined with other modifications [1]. This has been observed for two independent transductions of the c-erbB locus into acute transforming retroviruses [2, 3], as well as in c-erbB activation by promoter insertion during retroviral leukemogenesis [4]. The transforming gene of the feline sarcoma virus SM-FeSV represents another growth factor receptor tyrosine kinase, the CSF-1 receptor [5]. Oncogenic conversion by a retrovirus in this case (v-fms) involves more subtle structural alterations at the carboxyl terminus of the c-fms protooncogene [6].

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  1. Pier Paolo Di Fiore
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  1. Lombardi Cancer Research Center, Georgetown University School of Medicine, Washington, D.C., USA

    Robert B. Dickson  & Marc E. Lippman  & 

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Di Fiore, P.P., Kraus, M.H. (1991). Mechanisms involving an expanding erbB/EGF receptor family of tyrosine kinases in human neoplasia. In: Dickson, R.B., Lippman, M.E. (eds) Genes, Oncogenes, and Hormones. Cancer Treatment and Research, vol 61. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3500-3_7

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  • DOI: https://doi.org/10.1007/978-1-4615-3500-3_7

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