Journal
CHINESE JOURNAL OF CANCER
Volume 32, Issue 2, Pages 63-70Publisher
SUN YAT SEN UNIV MED SCI WHO
DOI: 10.5732/cjc.012.10098
Keywords
KRAS; RAS; oncogene; lung cancer
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Funding
- NIH [T32 GM007175]
- National Science Foundation Graduate Research Fellowship
- UCSF Academic Senate Research Grant
- Nan Tucker McEvoy Research Fund in Thoracic Oncology
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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.
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