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Items: 7

1.

Evidence that synthetic lethality underlies the mutual exclusivity of oncogenic KRAS and EGFR mutations in lung adenocarcinoma.

Unni AM, Lockwood WW, Zejnullahu K, Lee-Lin SQ, Varmus H.

Elife. 2015 Jun 5;4:e06907. doi: 10.7554/eLife.06907.

2.

Allosteric modulation of Ras and the PI3K/AKT/mTOR pathway: emerging therapeutic opportunities.

Hubbard PA, Moody CL, Murali R.

Front Physiol. 2014 Dec 16;5:478. doi: 10.3389/fphys.2014.00478. Review.

3.

Targeting the LKB1 tumor suppressor.

Zhao RX, Xu ZX.

Curr Drug Targets. 2014 Jan;15(1):32-52. Review.

4.

KRAS Mouse Models: Modeling Cancer Harboring KRAS Mutations.

O'Hagan RC, Heyer J.

Genes Cancer. 2011 Mar;2(3):335-43. doi: 10.1177/1947601911408080.

5.

Harnessing synthetic lethal interactions in anticancer drug discovery.

Chan DA, Giaccia AJ.

Nat Rev Drug Discov. 2011 May;10(5):351-64. doi: 10.1038/nrd3374. Review.

6.

Synthetic Lethality Induced by Loss of PKC δ and Mutated Ras.

Zhu T, Chen L, Du W, Tsuji T, Chen C.

Genes Cancer. 2010 Feb;1(2):142-51. doi: 10.1177/1947601909360989.

7.

Converting cancer mutations into therapeutic opportunities.

O'Brien T, Stokoe D.

EMBO Mol Med. 2009 Sep;1(6-7):297-9. doi: 10.1002/emmm.200900044.

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