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Title:
Absence of p21WAF1 cooperates with c-myc in bypassing Ras-induced senescence and enhances oncogenic cooperation | Oncogene
Description:
The absence of p21waf1 combined with an ectopic expression of c-myc prevents ras-induced senescence in mouse embryo fibroblasts. Extension of lifespan after c-myc transduction into p21-null cells was followed at later passages by apoptosis of a large fraction of c-myc-overexpressing p21-null cells. This apoptotic effect could be overridden by inactivation of the p53 tumor suppressor or oncogenic ras expression. Ras-induced inhibition of apoptosis is mediated by PI3K activation. These results suggest a functional relationship between ras and myc that may explain their oncogenic cooperation. The number of foci formed by myc+ras increased cooperatively in the absence of p21waf1. Thus, the reciprocal cooperation between myc and ras in a p21-null background during cellular immortalization lead to increased oncogenic cooperation between ras and myc.
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nature portfolio permissions reprints privacy policy c-myc-overexpressing p21-null cells biomedical research advertising social media nature bypassing ras-induced senescence author information authors trigger ros-induced autophagy author correspondence myc+ras increased cooperatively personal data p53 tumor suppressor ras-induced inhibition springerlink instant access data protection permissions enhances oncogenic cooperation p21-null cells cell growth differ increased oncogenic cooperation c-myc transduction privacy p21-null background oncogenic ras expression issue learn explore content subscription content ministerio de ciencia article carnero european economic area mouse embryo fibroblasts institutional subscriptions read munoz-alonso mj von der lehr catherine stevenson chair accepting optional cookies journals search log cellular immortalization lead c-myc franza jr br amancio carnero nucleic acids res cellular senescence manage preferences https oncogenic cooperation cancer cell proliferation
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headline:Absence of p21WAF1 cooperates with c-myc in bypassing Ras-induced senescence and enhances oncogenic cooperation
description:The absence of p21waf1 combined with an ectopic expression of c-myc prevents ras-induced senescence in mouse embryo fibroblasts. Extension of lifespan after c-myc transduction into p21-null cells was followed at later passages by apoptosis of a large fraction of c-myc-overexpressing p21-null cells. This apoptotic effect could be overridden by inactivation of the p53 tumor suppressor or oncogenic ras expression. Ras-induced inhibition of apoptosis is mediated by PI3K activation. These results suggest a functional relationship between ras and myc that may explain their oncogenic cooperation. The number of foci formed by myc+ras increased cooperatively in the absence of p21waf1. Thus, the reciprocal cooperation between myc and ras in a p21-null background during cellular immortalization lead to increased oncogenic cooperation between ras and myc.
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description:The absence of p21waf1 combined with an ectopic expression of c-myc prevents ras-induced senescence in mouse embryo fibroblasts. Extension of lifespan after c-myc transduction into p21-null cells was followed at later passages by apoptosis of a large fraction of c-myc-overexpressing p21-null cells. This apoptotic effect could be overridden by inactivation of the p53 tumor suppressor or oncogenic ras expression. Ras-induced inhibition of apoptosis is mediated by PI3K activation. These results suggest a functional relationship between ras and myc that may explain their oncogenic cooperation. The number of foci formed by myc+ras increased cooperatively in the absence of p21waf1. Thus, the reciprocal cooperation between myc and ras in a p21-null background during cellular immortalization lead to increased oncogenic cooperation between ras and myc.
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