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Campo DC Valor Lengua/Idioma
dc.creatorNegrotto, Soledad-
dc.creatorHu, Zhenbo-
dc.creatorAlcazar, Oscar-
dc.creatorNg, Kwok Peng-
dc.creatorTriozzi, Pierre-
dc.creatorLindner, Daniel-
dc.creatorRini, Brian-
dc.creatorSaunthararajah, Yogen-
dc.date2018-07-24T14:26:09Z-
dc.date2018-07-24T14:26:09Z-
dc.date2011-02-
dc.date2018-07-23T18:28:02Z-
dc.date.accessioned2019-04-29T15:53:13Z-
dc.date.available2019-04-29T15:53:13Z-
dc.date.issued2018-07-24T14:26:09Z-
dc.date.issued2018-07-24T14:26:09Z-
dc.date.issued2011-02-
dc.date.issued2018-07-23T18:28:02Z-
dc.identifierNegrotto, Soledad; Hu, Zhenbo; Alcazar, Oscar; Ng, Kwok Peng; Triozzi, Pierre; et al.; Noncytotoxic differentiation treatment of renal cell cancer; American Association for Cancer Research; Cancer Research; 71; 4; 2-2011; 1431-1441-
dc.identifier0008-5472-
dc.identifierhttp://hdl.handle.net/11336/52945-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/304655-
dc.descriptionCurrent drug therapy for metastatic renal cell cancer (RCC) results in temporary disease control but not cure, necessitating continued investigation into alternative mechanistic approaches. Drugs that inhibit chromatin-modifying enzymes involved in transcription repression (chromatin-relaxing drugs) could have a role, by inducing apoptosis and/or through differentiation pathways. At low doses, the cytosine analogue decitabine (DAC) can be used to deplete DNA methyl-transferase 1 (DNMT1), modify chromatin, and alter differentiation without causing apoptosis (cytotoxicity). Noncytotoxic regimens of DAC were evaluated for in vitro and in vivo efficacy against RCC cell lines, including a p53-mutated RCC cell line developed from a patient with treatment-refractory metastatic RCC. The cell division - permissive mechanism of action - absence of early apoptosis or DNA damage, increase in expression of HNF4α (hepatocyte nuclear factor 4a), a key driver associated with the mesenchymal to epithelial transition, decrease in mesenchymal marker expression, increase in epithelial marker expression, and late increase in cyclin-dependent kinase inhibitor CDKN1B (p27) protein - was consistent with differentiation-mediated cell-cycle exit. In vivo blood counts and animal weights were consistent with minimal toxicity of therapy. The distinctive mechanism of action of a dose and schedule of DAC designed for noncytotoxic depletion of DNMT1 suggests a potential role in treating RCC. ©2011 AACR.-
dc.descriptionFil: Negrotto, Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Cleveland Clinic; Estados Unidos-
dc.descriptionFil: Hu, Zhenbo. Cleveland Clinic; Estados Unidos-
dc.descriptionFil: Alcazar, Oscar. Cleveland Clinic; Estados Unidos-
dc.descriptionFil: Ng, Kwok Peng. Cleveland Clinic; Estados Unidos-
dc.descriptionFil: Triozzi, Pierre. Cleveland Clinic; Estados Unidos-
dc.descriptionFil: Lindner, Daniel. Cleveland Clinic; Estados Unidos-
dc.descriptionFil: Rini, Brian. Cleveland Clinic; Estados Unidos-
dc.descriptionFil: Saunthararajah, Yogen. Cleveland Clinic; Estados Unidos-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1158/0008-5472.CAN-10-2422-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://cancerres.aacrjournals.org/content/71/4/1431-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.subjectDECITABINE-
dc.subjectDIFFERENTIATION-
dc.subjectRENAL CARCINOMA-
dc.subjectCANCER TREATMENT-
dc.subjectInmunología-
dc.subjectMedicina Básica-
dc.subjectCIENCIAS MÉDICAS Y DE LA SALUD-
dc.titleNoncytotoxic differentiation treatment of renal cell cancer-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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