Cell transformation by the epidermal growth factor receptor and v-erbB.

Abstract

It has become increasingly apparent that growth factor receptors can function as oncogenic proteins and play causal roles in cell transformation. A prime example is the epidermal growth factor receptor (EGFR), which belongs to the ligand-activated tyrosine kinase receptor family and is overexpressed in certain human tumors. The transforming gene of avian erythroblastosis virus, v-erbB, encodes a truncated form of the EGFR whose kinase domain is constitutively activated by deletion of the ligand binding domain. Recent comparative studies of the v-erbB gene in different viral isolates have revealed that subtle sequence changes (point mutations, small deletions) can alter both the pathogenic spectrum of the virus and the range of cell types susceptible to transformation in vitro. Therefore, the possibility exists that similar, as-yet-unidentified, mutations may exist in the EGFR gene; if so, the EGFR may be an oncogenic factor in tumors other than those with which it has been associated to date.