GSBS Student Publications


Characterization of an angiosarcoma-inducing mutation in the erbB oncogene

GSBS Program

Biochemistry & Molecular Pharmacology

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Pathology; Department of Biochemistry and Molecular Biology



Document Type


Medical Subject Headings

Amino Acid Sequence; Animals; Base Sequence; Chickens; Cloning, Molecular; Gene Deletion; Hemangiosarcoma; Molecular Sequence Data; *Mutation; Phosphorylation; Proto-Oncogene Proteins; *Proto-Oncogenes; Receptor, Epidermal Growth Factor


Life Sciences | Medicine and Health Sciences


The erbB oncogenes of two transducing viruses that arose in chicken 5005 have been molecularly characterized. One of these viruses, AEV-5005, caused erythroblastosis. The other, AAV-5005, caused angiosarcoma. Both viruses had identical 5' junctions of viral and host sequences, indicating that both arose from the same proviral insertion. The erbB oncogenes of both viruses encoded transmembrane, kinase and C-terminal domains of the chicken epidermal growth factor receptor. The C-terminal domain of the AEV-5005 erbB was complete, whereas that of AAV-5005 contained a 59 amino acid internal deletion (amino acids 993-1051 of the chicken epidermal growth factor receptor). Oncogenicity tests using retroviral constructs containing the erbB sequences from AEV-5005 and AAV-5005 demonstrated that both erbB genes caused erythroblastosis and that the 59 amino acid deletion conferred the ability to induce angiosarcoma. The 59 amino acid deletion also caused increased levels of erbB autophosphorylation in cells grown in the presence of sodium orthovanadate.

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Citation: Oncogene. 1992 Oct;7(10):2025-30.

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