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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Carcinoma, Non-Small-Cell Lung / genetics*
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Carcinoma, Non-Small-Cell Lung / metabolism
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Carcinoma, Non-Small-Cell Lung / therapy
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Cell Transformation, Neoplastic / genetics
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Disease Susceptibility
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Gene Knockdown Techniques
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Genetic Therapy
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Humans
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Lung Neoplasms / genetics*
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Lung Neoplasms / metabolism
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Lung Neoplasms / therapy
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Mice
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Mutation*
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Neoplasms, Experimental / genetics
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Neoplasms, Experimental / metabolism
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Proto-Oncogene Proteins / genetics*
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins p21(ras)
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RNA, Small Interfering / genetics
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Signal Transduction
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ras Proteins / genetics*
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ras Proteins / metabolism
Substances
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KRAS protein, human
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Proto-Oncogene Proteins
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RNA, Small Interfering
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Proto-Oncogene Proteins p21(ras)
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ras Proteins