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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Detalles Bibliográficos
Autores principales: 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: Online Artículo Texto
Lenguaje:English
Publicado: 2018
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6039276/
https://www.ncbi.nlm.nih.gov/pubmed/29808010
http://dx.doi.org/10.1038/s41591-018-0022-x

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6039276/
https://www.ncbi.nlm.nih.gov/pubmed/29808010
http://dx.doi.org/10.1038/s41591-018-0022-x

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