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

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