Protein Kinases and Cancers

Dear Colleagues,

The regulation of protein function through phosphorylation is a major component of cellular signalling pathways, such as those that govern cell cycle progression, control gene expression or determine whether a cell survives or dies. In humans, the phosphorylation of proteins is catalysed by over 500 protein kinases, most of which specifically modify either Ser/Thr or Tyr side chains. Their catalytic activities are regulated through molecular mechanisms that are dysregulated in cancer by mutations that cause uncontrolled kinase activity. Tumours that harbour such mutations can be addicted to the activity of a single protein kinase, and kinase inhibitors have recently become a successful class of cancer therapeutic.

Despite rapid progress in the field of “Protein Kinases and Cancer”, opportunities remain for further developments that would transform our understanding of cancer and its treatment. For example, most research is focused on a small subset of human kinases and the biological functions of many cancer-relevant kinases have yet to be explored. This needs to be corrected if we are to fully exploit the potential of protein kinases in cancer therapy. A second example is the trend in drug discovery programmes towards developing approaches to overcome resistance to current therapeutics, such as allosteric kinase inhibitors. This innovative approach takes advantage of developments in our understanding of the structural mechanisms of kinase regulation.

We aim to stimulate discussion by bringing together expert opinion and new science from across the field in a Special Issue of Cancers. We welcome submissions that cover any relevant topic, including protein kinases and non-oncogene addiction; non-canonical protein kinases; protein kinase structure and dynamics; mechanisms of dysregulation in cancer; small molecule inhibitors of protein kinases; allostery in protein kinases; the future of protein kinase therapeutics.

Prof. Richard Bayliss
Dr. Sharon Yeoh
Guest Editors

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