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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2003-9-22
pubmed:abstractText
Adenovirus synthesize proteins that interact with oncogene and tumor suppressor gene products to set the cell for virus replication. Mutant viruses defective in these functions replicate selectively in cancer cells and represent new tools to treat cancer. We report a selectivity strategy based on deletions of adenovirus Virus-Associated (VA) RNAs. In normal cells, these RNAs are necessary for virus replication because they inactivate the RNA-dependent protein kinase protein kinase R, a kinase that otherwise would block protein translation in response to infection. However, downstream effectors of Ras can also inactivate protein kinase R, and therefore, the need for VA RNA genes should be bypassed in cells with an active Ras pathway. We demonstrate here that a VAI RNA mutant presents a Ras-dependent replication and can be used for oncolytic virotherapy of pancreatic tumors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5544-50
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Ras-dependent oncolysis with an adenovirus VAI mutant.
pubmed:affiliation
Translational Research Laboratory, Institut Català d'Oncologia, 08907, L'Hospitalet, Barcelona, Spain.
pubmed:publicationType
Journal Article