Targeting wild-type KRAS amplified gastroesophageal cancer through combined MEK and SHP2

The role of KRAS, when activated through canonical mutations, has been well established in cancer(1). Here we explore a secondary means of KRAS activation in cancer, focal high-level amplification of the KRAS gene in the absence of coding mutations. These amplifications occur most commonly in esopha...

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Publicado no:Nat Med
Main Authors: Wong, Gabrielle S., Zhou, Jin, Liu, Jie Bin, Wu, Zhong, Xu, Xinsen, Li, Tianxia, Xu, David, Schumacher, Steven E., Puschhof, Jens, McFarland, James, Zou, Charles, Dulak, Austin, Henderson, Les, Xu, Peng, O’Day, Emily, Rendak, Rachel, Liao, Wei-li, Cecchi, Fabiola, Hembrough, Todd, Schwartz, Sarit, Szeto, Christopher, Rustgi, Anil K., Wong, Kwok-Kin, Diehl, J. Alan, Jensen, Karin, Graziano, Francesco, Ruzzo, Annamaria, Fereshetian, Shaunt, Mertins, Philipp, Carr, Steven A., Beroukhim, Rameen, Nakamura, Kenichi, Oki, Eiji, Watanabe, Masayuki, Baba, Hideo, Imamura, Yu, Catenacci, Daniel, Bass, Adam J.
Formato: Artigo
Idioma:Inglês
Publicado em: 2018
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Article
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC6039276/
https://ncbi.nlm.nih.gov/pubmed/29808010
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/s41591-018-0022-x
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