期刊
CANCER CELL
卷 18, 期 1, 页码 63-73出版社
CELL PRESS
DOI: 10.1016/j.ccr.2010.05.025
关键词
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资金
- Ministry of Science and Innovation (MICINN) [SAF2006-11773, CSD2007-00017]
- Autonomous Community of Madrid [GR/SAL/0587/2004, S2006/BIO-0232, GR/SAL/0349/2004]
- Fundacion de la Mutua Madrilena
- EU [LSHG-CT-2007-037665]
- Fondo de Investigacion Sanitaria [P1061631, PI042124]
- INSERM
- Association pour la Recherche contra le Cancer (Region Aquitaine)
We have unveiled a synthetic lethal interaction between K-Ras oncogenes and Cdk4 in a mouse tumor model that closely recapitulates human non-small cell lung carcinoma (NSCLC). Ablation of Cdk4, but not Cdk2 or Cdk6, induces an immediate senescence response only in lung cells that express an endogenous K-Ras oncogene. No such response occurs in lungs expressing a single Cdk4 allele or in other K-Ras-expressing tissues. More importantly, targeting Cdk4 alleles in advanced tumors detectable by computed tomography scanning also induces senescence and prevents tumor progression. These observations suggest that robust and selective pharmacological inhibition of Cdk4 may provide therapeutic benefit for NSCLC patients carrying K-RAS oncogenes.
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