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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Publicat a:Nat Med
Autors principals: 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.
Format: Artigo
Idioma:Inglês
Publicat: 2018
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Article
Accés en línia: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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