Induction of renal adenocarcinoma by a nonmutated erbB oncogene

summary, we have demonstrated a new disease poten- tial for the nonmutatederbB oncogene. Specifically, we have shown that a virally expressed C-terminal complete erbB induces a 100% incidence ofrenal neoplasia. Wethank Steven Theroux for the Ala-477/478 and Glu-477/478 point mutants, David Brownfor assistance with oncogenicity tests, and Laura Rooney for histologic preparation of tissues. This work was supported by Public Health Service research grants CA27223 and CA23086 to H.L.R. and CA58396 to R.J.D.REFERENCES1. Beug, H., M. J. Hayman, M. B. Raines, H. J. Kung, and B.Vennstrom. 1986. Rous-associated virus 1-induced erythroleu-kemiccells exhibit aweaklytransformedphenotypeinvitroandrelease c-erbB-containing retroviruses unable to transform fi-broblasts. J. Virol. 57:1127-1138.2. Breyer, M.D., R. Reyadh, and J. A. Breyer. 1990. Segmentaldistribution of epidermal growth factor binding sites in rabbitnephron. Am.J. Physiol. 259:F553-F558.3. Carr, J. G. 1956. Renal adenocarcinoma induced by fowlleukemiavirus. Br. J. Cancer 10:379-383.4. Choi, O.-R., C. Trainor, T. Graf, H. Beug, and J. D. Engel.1986. A single amino acid substitution in v-erbB confers athermolabile phenotype to ts167 avian erythroblastosis virus-transformed erythroid cells. Mol. Cell. Biol. 6:1751-1759.5. Countaway, J. L., A. C. Nairn, and R. J. Davis. 1992. Mecha-nismofdesensitization ofthe epidermal growth factor receptorprotein-tyrosine kinase. J. Biol. Chem. 267:1129-1140.6. Damm,K., H. Beug,T.Graf, andB.Vennstrom. 1987. Asinglepoint mutation in erbA restores the erythroid transformingpotential of a mutant avian erythroblastosis virus (AEV)defec-tive in both erbA anderbB oncogenes. EMBOJ. 6:375-382.7.