Most common mechanisms of resistance of multikinase inhibitors MKIs Biology Diagrams Targeting the mitotic checkpoint for cancer therapy with NMS-P715, an inhibitor of MPS1 kinase. Cancer Res 2010; 70 : 10255-10264. Article CAS PubMed Google Scholar
This was accomplished by combining CDK4/6i with additional CIN-inducing agents, including a bromodomain and extraterminal repeat (BET) inhibitor and mitotic kinase inhibitors. As the inhibition of many mitotic kinases is highly toxic, we identified Nima-related kinase 2 (NEK2) as a potential therapeutic target that could be combined with CDK4/6i.
Discovery of Potent and Selective MNK Kinase Inhibitors for the ... Biology Diagrams
In prostate cancers, the abundance of the tumor suppressor PDCD4 is inversely correlated with response to the antiandrogen (also known as an androgen receptor inhibitor) enzalutamide. Zhang et al. found that PDCD4 is repressed by the mitotic kinase PLK1, which enabled the activity of cell survival pathways that are androgen independent. In Anti-mitotic therapies in cancer J Cell Biol. 2019 Jan 7;218(1) :10-11. doi Aurora Kinase B / antagonists & inhibitors Aurora Kinase B / genetics Aurora Kinase B / metabolism Neoplasms / drug therapy* Neoplasms / genetics Neoplasms / metabolism
The development of mitotic kinase inhibitors came as an outgrowth of studies on the molecular mechanisms of the cell cycle in the 1990s [38-40], which promised the development of precise inhibitors of mitosis without the toxic sequelae of classical chemotherapeutics. Yet for all the initial excitement, mitotic kinase inhibitors have now been Mitosis checkpoint kinase (CHK) inhibitors (including LY2603618) These agents act on the mitotic process, a proven target for anti-neoplastic therapy. It will be important for the development of these agents to evaluate the potential advantages over available mitotic inhibitors. It is likely that patient selection will hold a key to Protein kinases are crucial targets for cancer treatment as they orchestrate important signals for oncogenesis and are often aberrantly activated owing to genomic alterations. In the past two
mitotic therapies in cancer Biology Diagrams
Kinase and BET inhibitors together clamp inhibition of PI3K signaling and overcome resistance to therapy Cancer Cell , 27 ( 2015 ) , pp. 837 - 851 , 10.1016/j.ccell.2015.05.006 View PDF View article View in Scopus Google Scholar