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Comment
. 2014 Jul 3;158(1):11-2.
doi: 10.1016/j.cell.2014.06.021.

YAP1 takes over when oncogenic K-Ras slumbers

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Free article
Comment

YAP1 takes over when oncogenic K-Ras slumbers

Florian R Greten. Cell. .
Free article

Abstract

It is of great therapeutic importance to understand why tumors relapse after the failure of therapies targeting oncogenes to which cancer cells are addicted. In this issue, Kapoor et al. and Shao et al. identify the transcriptional coactivator YAP1 as a central driver of compensation for the loss of K-Ras signaling in K-Ras-dependent cancers.

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  • Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer.
    Kapoor A, Yao W, Ying H, Hua S, Liewen A, Wang Q, Zhong Y, Wu CJ, Sadanandam A, Hu B, Chang Q, Chu GC, Al-Khalil R, Jiang S, Xia H, Fletcher-Sananikone E, Lim C, Horwitz GI, Viale A, Pettazzoni P, Sanchez N, Wang H, Protopopov A, Zhang J, Heffernan T, Johnson RL, Chin L, Wang YA, Draetta G, DePinho RA. Kapoor A, et al. Cell. 2014 Jul 3;158(1):185-197. doi: 10.1016/j.cell.2014.06.003. Epub 2014 Jun 19. Cell. 2014. PMID: 24954535 Free PMC article.
  • KRAS and YAP1 converge to regulate EMT and tumor survival.
    Shao DD, Xue W, Krall EB, Bhutkar A, Piccioni F, Wang X, Schinzel AC, Sood S, Rosenbluh J, Kim JW, Zwang Y, Roberts TM, Root DE, Jacks T, Hahn WC. Shao DD, et al. Cell. 2014 Jul 3;158(1):171-84. doi: 10.1016/j.cell.2014.06.004. Epub 2014 Jun 19. Cell. 2014. PMID: 24954536 Free PMC article.

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