- Author:
Peter M K WESTCOTT
1
;
Minh D TO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Carcinoma, Non-Small-Cell Lung; genetics; metabolism; therapy; Cell Transformation, Neoplastic; genetics; Disease Susceptibility; Gene Knockdown Techniques; Genetic Therapy; Humans; Lung Neoplasms; genetics; metabolism; therapy; Mice; Mutation; Neoplasms, Experimental; genetics; metabolism; Proto-Oncogene Proteins; genetics; metabolism; Proto-Oncogene Proteins p21(ras); RNA, Small Interfering; genetics; Signal Transduction; ras Proteins; genetics; metabolism
- From:Chinese Journal of Cancer 2013;32(2):63-70
- CountryChina
- Language:English
- Abstract: Mutational activation of KRAS is a common oncogenic event in lung cancer and other epithelial cancer types. Efforts to develop therapies that counteract the oncogenic effects of mutant KRAS have been largely unsuccessful, and cancers driven by mutant KRAS remain among the most refractory to available treatments. Studies undertaken over the past decades have produced a wealth of information regarding the clinical relevance of KRAS mutations in lung cancer. Mutant Kras-driven mouse models of cancer, together with cellular and molecular studies, have provided a deeper appreciation for the complex functions of KRAS in tumorigenesis. However, a much more thorough understanding of these complexities is needed before clinically effective therapies targeting mutant KRAS-driven cancers can be achieved.