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. 2017 Sep 11;37(1):128–138. doi: 10.1038/onc.2017.316

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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The KRAS/TGF-β/p15Ink4b pathway controls the cell fate. Although oncogenic KRAS activates the proliferative signals, it also stimulates the TGF-β expression through MEK-EGR1 cascade. TGF-β further activates Cdkn2b expression via Smads component of TGF-β pathway. The p15Ink4b encoded by Cdkn2b gene together with p16Ink4a encoded by Cdkfn2a inhibit the Rb phosphorylation and activate Rb to induce cellular senescence and prevent tumor formation. However, when both Cdkn2a and Cdkn2b are inactivated, Rb is phosphorylated by CDK4/6 and make the cells encompass cellular senescence, which allow tumor formation.