{"id":61062,"date":"2018-03-09T22:48:55","date_gmt":"2018-03-09T22:48:55","guid":{"rendered":"https:\/\/www.deberes.net\/tesis\/sin-categoria\/funciones-de-p21-en-la-regulacion-genica-y-en-la-apoptosis-por-inhibidores-de-tirosina-quinasa-estudio-en-modelos-de-cancer-colorectal-y-leucemia-mieloide\/"},"modified":"2018-03-09T22:48:55","modified_gmt":"2018-03-09T22:48:55","slug":"funciones-de-p21-en-la-regulacion-genica-y-en-la-apoptosis-por-inhibidores-de-tirosina-quinasa-estudio-en-modelos-de-cancer-colorectal-y-leucemia-mieloide","status":"publish","type":"post","link":"https:\/\/www.deberes.net\/tesis\/biologia-celular\/funciones-de-p21-en-la-regulacion-genica-y-en-la-apoptosis-por-inhibidores-de-tirosina-quinasa-estudio-en-modelos-de-cancer-colorectal-y-leucemia-mieloide\/","title":{"rendered":"Funciones de p21 en la regulaci\u00f3n g\u00e9nica y en la apoptosis por inhibidores de tirosina-quinasa. estudio en modelos de c\u00e1ncer colorectal y leucemia mieloide"},"content":{"rendered":"<h2>Tesis doctoral de <strong> Nuria Ferrandiz Diaz <\/strong><\/h2>\n<p>Trabajos comparativos realizados en una l\u00ednea celular isog\u00e9nica derivada de hct116 (hct116p21-\/-) han servido para describir el papel de p21 como protector de la apoptosis contra distintos tipos de f\u00e1rmacos y est\u00edmulos. Nosotros nos preguntamos si p21 tmabi\u00e9n proteger\u00eda de la apoptosis inducida por f\u00e1rmacos no genot\u00f3xicos como son los inhibidores tirosina quinasa (imatinib y gefitinib), utilizados en la terapia contra el c\u00e1ncer. Nosotros hemos encontrado que las c\u00e9lulas deficientes en p21 son m\u00e1s sensibles a los inhibidores tirosina-quinasa que las c\u00e9lulas parentales. Sin embargo, la expresi\u00f3n inducible de p21 en hct116p21-\/-, no rescata a las c\u00e9lulas de la hipersensibilidad a imatinib y adriamicina. Adem\u00e1s, la represi\u00f3n  de la expresi\u00f3n end\u00f3gena de p21 en hct116wt por c-myc o por el silenciamiento con sirna, no incrementa la sensibilidad de las c\u00e9lulas parentales (hct116wt) a f\u00e1rmacos tirosina-quinasa. Nosotros hemos encontrado que las c\u00e9lulas hct116p21-\/- presentan mayor expresi\u00f3n, actividad y estabilidad de la prote\u00edna p53, comparando con las c\u00e9lulas parentales. Adem\u00e1s, la expresi\u00f3n de un dominante negativo de p53 o el silenciamiento de la expresi\u00f3n de p53 en hct116p21-\/- rescata a las c\u00e9lulas del fenotipo  hipersensibles a imatinib y adriamicina. Asimismo, las l\u00edneas deficientes en p21 de muestran mayores niveles de actividad de las prote\u00ednas tirosina-quinasa como son c-abl, c-src, akt y erk1\/2. nosotros concluimos que la apoptosis mediada por imatinib es parcialmente dependiente de p53 en la l\u00ednea celular hct116p21-\/- y que la alta actividad de p53 y no la ausencia de p21, es el principal mecanismo por el cual las c\u00e9lulas hct116p21-\/- son hipersensibles a f\u00e1rmacos tumorales. Por lo tanto, muchas de las conclusiones extra\u00eddas del papel de p21 en apoptosis en el modelo celular hct116p21-\/- deber\u00edan ser revaluadas. Sin embargo, realizamos otro estudio independiente en una l\u00ednea celular derivada de leucemia mieloide cr\u00f3nica (k<\/p>\n<p>&nbsp;<\/p>\n<h3>Datos acad\u00e9micos de la tesis doctoral \u00ab<strong>Funciones de p21 en la regulaci\u00f3n g\u00e9nica y en la apoptosis por inhibidores de tirosina-quinasa. estudio en modelos de c\u00e1ncer colorectal y leucemia mieloide<\/strong>\u00ab<\/h3>\n<ul>\n<li><strong>T\u00edtulo de la tesis:<\/strong>\u00a0 Funciones de p21 en la regulaci\u00f3n g\u00e9nica y en la apoptosis por inhibidores de tirosina-quinasa. estudio en modelos de c\u00e1ncer colorectal y leucemia mieloide <\/li>\n<li><strong>Autor:<\/strong>\u00a0 Nuria Ferrandiz Diaz <\/li>\n<li><strong>Universidad:<\/strong>\u00a0 Cantabria<\/li>\n<li><strong>Fecha de lectura de la tesis:<\/strong>\u00a0 26\/10\/2007<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<h3>Direcci\u00f3n y tribunal<\/h3>\n<ul>\n<li><strong>Director de la tesis<\/strong>\n<ul>\n<li>Javier Le\u00f3n Serrano<\/li>\n<\/ul>\n<\/li>\n<li><strong>Tribunal<\/strong>\n<ul>\n<li>Presidente del tribunal: Jos\u00e9 Miguel Ortiz Melon <\/li>\n<li>Jorge Martin Perez (vocal)<\/li>\n<li>Neus Agell Jane (vocal)<\/li>\n<li>Jos\u00e9 Carlos Rodriguez Rey (vocal)<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Tesis doctoral de Nuria Ferrandiz Diaz Trabajos comparativos realizados en una l\u00ednea celular isog\u00e9nica derivada de hct116 (hct116p21-\/-) han servido [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"site-sidebar-layout":"default","site-content-layout":"","ast-site-content-layout":"","site-content-style":"default","site-sidebar-style":"default","ast-global-header-display":"","ast-banner-title-visibility":"","ast-main-header-display":"","ast-hfb-above-header-display":"","ast-hfb-below-header-display":"","ast-hfb-mobile-header-display":"","site-post-title":"","ast-breadcrumbs-content":"","ast-featured-img":"","footer-sml-layout":"","theme-transparent-header-meta":"","adv-header-id-meta":"","stick-header-meta":"","header-above-stick-meta":"","header-main-stick-meta":"","header-below-stick-meta":"","astra-migrate-meta-layouts":"default","ast-page-background-enabled":"default","ast-page-background-meta":{"desktop":{"background-color":"var(--ast-global-color-4)","background-image":"","background-repeat":"repeat","background-position":"center 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