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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1981-5-28
pubmed:abstractText
Unlike other RNA tumor viruses, avian leukosis viruses (which cause lymphomas and occasionally other neoplasms) lack discrete "transforming genes". We have analyzed the virus-related DNA and RNA of avian leukosis virus (ALV)-induced tumors in an attempt to gain insight into the mechanism of ALV oncogenesis. Our results show that viral gene products are not required for maintenance of neoplastic transformation. Primary and metastatic tumors are clonal and thus presumably derived from a single infected cell. Most importantly, tumors from different birds have integration sites in common. Tumor cells synthesize discrete new poly(A) RNAs consisting of viral sequences covalently linked to cellular sequences. These RNA species are expressed at high levels in tumor cells. Our results suggest that in lymphoid tumors, an ALV provirus is integrated adjacent to a specific cellular gene, and the insertion of the viral promoter adjacent to this gene results in its enhanced expression, leading to neoplasia. These results have potentially important implications for the mechanism of non-viral carcinogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
323-34
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Avian leukosis virus-induced tumors have common proviral integration sites and synthesize discrete new RNAs: oncogenesis by promoter insertion.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.