Registro completo de metadatos
Campo DC Valor Lengua/Idioma
dc.creatorBlanco, R. (R.)
dc.creatorIwakawa, R. (R.)
dc.creatorTang, M. (Moying)
dc.creatorKohno, T. (Takashi)
dc.creatorAngulo, B. (B.)
dc.creatorPio, R. (Rubén)
dc.creatorMontuenga, L.M. (Luis M.)
dc.creatorMinna, J.D. (John D.)
dc.creatorYokota, J. (Jun)
dc.creatorSanchez-Cespedes, M. (Montserrat)
dc.date.accessioned2010-10-21T07:48:55Z-
dc.date.available2010-10-21T07:48:55Z-
dc.date.issued2009-03-12-
dc.identifier.citationBlanco R, Iwakawa R, Tang M, Kohno T, Angulo B, Pio R, et al. A gene-alteration profile of human lung cancer cell lines. Hum Mutat 2009 Aug;30(8):1199-1206.es_ES
dc.identifier.issn1059-7794-
dc.identifier.urihttp://hdl.handle.net/10171/13568-
dc.description.abstractABSTRACT: Aberrant proteins encoded from genes altered in tumors drive cancer development and may also be therapeutic targets. Here we derived a comprehensive gene-alteration profile of lung cancer cell lines. We tested 17 genes in a panel of 88 lung cancer cell lines and found the rates of alteration to be higher than previously thought. Nearly all cells feature inactivation at TP53 and CDKN2A or RB1, whereas BRAF, MET, ERBB2, and NRAS alterations were infrequent. A preferential accumulation of alterations among histopathological types and a mutually exclusive occurrence of alterations of CDKN2A and RB1 as well as of KRAS, epidermal growth factor receptor (EGFR), NRAS, and ERBB2 were seen. Moreover, in nonsmall- cell lung cancer (NSCLC), concomitant activation of signal transduction pathways known to converge in mammalian target of rapamycin (mTOR) was common. Cells with single activation of ERBB2, PTEN, or MET signaling showed greater sensitivity to cell-growth inhibition induced by erlotinib, LY294002, and PHA665752, respectively, than did cells featuring simultaneous activation of these pathways, underlining the need for combined therapeutic strategies in targeted cancer treatments. In conclusion, our gene-alteration landscape of lung cancer cell lines provides insights into how gene alterations accumulate and biological pathways interact in cancer. Hum Mutat 30, 1199–1206, 2009. & 2009Wiley-Liss, Inc.es_ES
dc.language.isoenges_ES
dc.publisherHuman Mutationes_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.subjectLung canceres_ES
dc.subjectOncogeneses_ES
dc.subjectTumor suppressorses_ES
dc.subjectTyrosine kinase inhibitorses_ES
dc.titleA gene-alteration profile of human lung cancer cell lineses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1002/humu.21028es_ES

Ficheros en este registro:
Fichero: 
montuengaagenealteration2009.pdf
Descripción: 
Tamaño: 
313,51 kB
Formato: 
Adobe PDF


Los ítems de Dadun están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.