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Title: v-src induces clonal sarcomas and rapid metastasis following transduction with a replication-defective retrovirus

Journal Article · · Proceedings of the National Academy of Sciences of the United States of America; (USA)
;  [1]
  1. Univ. of California, Berkeley (USA)

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. The authors 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 {approx} 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.

DOE Contract Number:
AC03-76SF00098
OSTI ID:
7138300
Journal Information:
Proceedings of the National Academy of Sciences of the United States of America; (USA), Vol. 86:24; ISSN 0027-8424
Country of Publication:
United States
Language:
English

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