Journal
CANCER CELL
Volume 19, Issue 5, Pages 652-663Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2011.04.002
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Funding
- EU [LSHG-CT-2007-037665]
- European Research Council [250297]
- Spanish Ministry of Science and Innovation [SAF2006-11773, CSD2007-00017]
- Autonomous Community of Madrid [GR/SAL/0587/2004, S2006/BIO-0232]
- Fundacion de la Mutua Madrilena del Automovil
- Austrian Scientific Research Fund [SEB 021]
- Canadian Institutes of Health Research [MOP-97801]
- Fondo de Investigaciones Sanitarias
- FEBS Long-Term Fellowship
- Instituto de Salud Carlos III
- European Research Council (ERC) [250297] Funding Source: European Research Council (ERC)
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We have investigated the role of individual members of the Raf/Mek/Erk cascade in the onset of K-Ras oncogene-driven non-small cell lung carcinoma (NSCLC). Ablation of Erk1 or Erk2 in K-Ras oncogene-expressing lung cells had no significant effect due to compensatory activities. Yet, elimination of both Erk kinases completely blocked tumor development. Similar results were obtained with Mek kinases. Ablation of B-Raf had no significant effect on tumor development. However, c-Raf expression was absolutely essential for the onset of NSCLC. Interestingly, concomitant elimination of c-Raf and B-Raf in adult mice had no deleterious consequences for normal homeostasis. These results indicate that c-Raf plays a unique role in mediating K-Ras signaling and makes it a suitable target for therapeutic intervention.
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