david gramp and girl and dating - Validating aurora b as an anticancer drug target

This work is licensed under the Creative Commons Attribution-Non Commercial-No Derivative Works 3.0 Unported License.To view a copy of this license, visit strategy of clinically targeting cancerous cells at their most vulnerable state during mitosis has instigated numerous studies into the mitotic cell death (MCD) pathway.

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We then devised strategies to inhibit these anti-cancer drug targets and selected a set of targets that are amenable to inhibition by small molecules, antibodies and synthetic peptides.

We validated the predicted drug targets by showing strong anti-proliferative effects of both synthetic peptide and small molecule inhibitors against our predicted targets.

This leaves a vast space of the protein universe unexploited by cancer drugs.

Hence, there is an urgent need for the identification and validation of new cancer-relevant targets.

As the hallmark of cancer revolves around cell-cycle deregulation, it is not surprising that antimitotic therapies are effective against the abnormal proliferation of transformed cells.

Moreover, these antimitotic drugs are also highly selective and sensitive.

Our studies predict that drug-resistant Aurora B mutants are likely to arise during clinical treatment.

Furthermore, because the plasticity of the ATP-binding pocket renders Aurora B insensitive to multiple inhibitors, our observations indicate that the drug-resistant Aurora B mutants should be exploited as novel drug targets.

These observations led to a number of programs among academic and pharmaceutical organizations to discovering small molecule Aurora kinase inhibitors as anti-cancer drugs.

This review will summarize the known Aurora kinase inhibitors currently in the clinic, and discuss the current and future directions.

Three mutations map to residues in the ATP-binding pocket that are distinct from the “gatekeeper” residue.

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