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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محفوظ في:
التفاصيل البيبلوغرافية
الحاوية / القاعدة:Nat Med
المؤلفون الرئيسيون: 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.
التنسيق: Artigo
اللغة:Inglês
منشور في: 2018
الموضوعات:
Article
الوصول للمادة أونلاين: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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