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http://hdl.handle.net/10261/6284
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dc.contributor.author | Cobaleda, César | - |
dc.contributor.author | Sánchez García, Isidro | - |
dc.date.accessioned | 2008-07-31T16:50:09Z | - |
dc.date.available | 2008-07-31T16:50:09Z | - |
dc.date.issued | 2000 | - |
dc.identifier.citation | Blood 95(3): 731-737 (2000) | en_US |
dc.identifier.issn | 0006-4971 | - |
dc.identifier.uri | http://hdl.handle.net/10261/6284 | - |
dc.description.abstract | One major obstacle to the effective treatment of cancer is to distinguish between tumor cells and normal cells. The chimeric molecules created by cancer-associated chromosomal abnormalities are ideal therapeutic targets because they are unique to the disease. We describe the use of a novel approach based on the catalytic RNA subunit of RNase P to destroy specifically the tumor-specific fusion genes created as a result of chromosome abnormalities. Using as a target model the abnormal BCR-ABL p190 and p210 products, we constructed M1-RNA with guide sequences that recognized the oncogenic messengers at the fusion point (M1-p190-GS and M1-p210-GS). To test the effectiveness and the specificity of M1-p190-GS and M1-p210-GS, we studied in vitro and in vivo effects of these RNA enzymes against BCR-ABL(p190) and BCR-ABL(p210), bearing in mind that both fusion genes share the ABL sequence but differ in the sequence coming from the BCR gene. We showed that M1-p190-GS and M1-p210-GS can act as sequence-specific endonucleases and can exclusively cleave target RNA that forms a base pair with the guide sequence (GS). We also demonstrated that when M1-p190-GS and M1-p210-GS were expressed in proper mammalian cell models, they abolished the effect of BCR-ABL by specifically decreasing the amount of the target BCR-ABL mRNA and preventing the function of the BCR-ABL oncogenes. These data clearly demonstrate the usefulness of the catalytic activity of M1-GS RNA to cleave specifically the chimeric molecules created by chromosomal abnormalities in human cancer and to represent a novel approach to cancer treatment. | - |
dc.description.sponsorship | Supported by the European Commission (BMH4-CT96-0375); the DGCYT (UE96-0041, PB96-0816, and 1FD97-0360); the Fundación Científica of the AECC; the Junta de Castilla y León (CS12/99); the FIS (99/0935); and the National Institutes of Health (1 R01 CA79955-01). C.C. is a fellow of the Fundación Ferrer Investigación. | - |
dc.format.extent | 268944 bytes | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | en_US |
dc.publisher | American Society of Hematology | - |
dc.rights | closedAccess | en_US |
dc.title | In vivo inhibition by a site-specific catalytic RNA subunit of RNase P designed against the BCR-ABL oncogenic products: a novel approach for cancer treatment | en_US |
dc.type | artículo | en_US |
dc.description.peerreviewed | Peer reviewed | en_US |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.fulltext | No Fulltext | - |
item.languageiso639-1 | en | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | none | - |
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