v-src induces clonal sarcomas and rapid metastasis following transduction with a replication-defective retrovirus.
Proc Natl Acad Sci U S A
; 86(24): 10123-7, 1989 Dec.
Article
in En
| MEDLINE
| ID: mdl-2557619
ABSTRACT
v-src is an effective carcinogen when expressed from Rous sarcoma virus (RSV) in vivo. Whereas RSV tumors require sustained oncogene expression, their growth is largely a balance between viral recruitment of tissues and host immune destruction of infected cells. We have therefore examined the tumorigenic potential of v-src in the absence of viral recruitment and viral antigen expression. v-src was introduced with high efficiency into chicken wing web tissues using replication-defective (rd) retroviral vectors. Clonal sarcomas were induced rapidly, and, furthermore, v-src potentiated metastatic progression in approximately 0.1%-1% of tumor clones with unexpectedly short latency. rd vectors proved effective not only in transducing v-src into tissues but also as insertional markers of tumor clonality. The rd vector present in most primary and metastatic tumors was a highly truncated form of RSV derived by viral transmission of spliced v-src mRNA; this vector should thus avoid viral recruitment and host anti-viral immune reaction through its complete lack of viral structural genes. Under such conditions v-src maintains strong carcinogenicity in vivo when restricted to clonal tumor growth and can confer rapid metastatic potential on a discrete subset of tumor clones.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Oncogenes
/
Transduction, Genetic
/
Gene Expression
/
Sarcoma, Avian
/
Avian Sarcoma Viruses
/
Defective Viruses
Limits:
Animals
Language:
En
Journal:
Proc Natl Acad Sci U S A
Year:
1989
Document type:
Article