夫拉平度对人宫颈癌CasKi细胞裸鼠皮下种植瘤生长的抑制作用研究(4)
[10] Matthew P. Swaffer， Andrew W. Jones， Helen R. Flynn， et al. I CDK Substrate Phosphorylation and Ordering the Cell Cycle [J]. Cell. 2016， 167(7)： 1750-1761.
[11] CROWN J.CDK8： a new breast cancer target[J]. Oncotar get， 2017， 8 (9) ：14269-14270.
[12] JABBOUR-LEUNG NA， CHEN X， BUI T， et al. Sequential combination therapy of CDK inhibition and doxorubicin is synthetically lethal in p53-mutant triple-negative breast cancer[J]. Mol Cancer Ther， 2016， 15(4)：593-607.
[13] Nicole M. Davis， Melissa Sokolosky， Kristin Stadelman， et al. Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer： possibilities for therapeutic intervention[J]. Oncotarget， 2014， 5(13)： 4603–4650.
[14] Xavier Bisteau， Sabine Paternot， Bianca Colleoni，et al. CDK4 T172 Phosphorylation Is Central in a CDK7-Dependent Bidirectional CDK4/CDK2 Interplay Mediated by p21 Phosphorylation at the Restriction Point[J].PLoS Genet， 2013，9(5)： e1003546.
[15] C Norez， C Vandebrouck， J Bertrand， et al. Roscovitine is a proteostasis regulator that corrects the trafficking defect of F508del-CFTR by a CDK-independent mechanism[J].Br J Pharmacol， 2014， 171(21)： 4831-4849.
(收稿日期：2018-01-22), 百拇医药(周焕芹)
[11] CROWN J.CDK8： a new breast cancer target[J]. Oncotar get， 2017， 8 (9) ：14269-14270.
[12] JABBOUR-LEUNG NA， CHEN X， BUI T， et al. Sequential combination therapy of CDK inhibition and doxorubicin is synthetically lethal in p53-mutant triple-negative breast cancer[J]. Mol Cancer Ther， 2016， 15(4)：593-607.
[13] Nicole M. Davis， Melissa Sokolosky， Kristin Stadelman， et al. Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer： possibilities for therapeutic intervention[J]. Oncotarget， 2014， 5(13)： 4603–4650.
[14] Xavier Bisteau， Sabine Paternot， Bianca Colleoni，et al. CDK4 T172 Phosphorylation Is Central in a CDK7-Dependent Bidirectional CDK4/CDK2 Interplay Mediated by p21 Phosphorylation at the Restriction Point[J].PLoS Genet， 2013，9(5)： e1003546.
[15] C Norez， C Vandebrouck， J Bertrand， et al. Roscovitine is a proteostasis regulator that corrects the trafficking defect of F508del-CFTR by a CDK-independent mechanism[J].Br J Pharmacol， 2014， 171(21)： 4831-4849.
(收稿日期：2018-01-22), 百拇医药(周焕芹)