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dc.contributor.authorBrognard, J
dc.contributor.authorHunter, Tony
dc.date.accessioned2011-01-20T17:07:45Z
dc.date.available2011-01-20T17:07:45Z
dc.date.issued2010-11-29
dc.identifier.citationProtein kinase signaling networks in cancer. 2010: Curr Opin Genet Deven
dc.identifier.issn1879-0380
dc.identifier.pmid21123047
dc.identifier.doi10.1016/j.gde.2010.10.012
dc.identifier.urihttp://hdl.handle.net/10541/120106
dc.description.abstractProtein kinases orchestrate the activation of signaling cascades in response to extracellular and intracellular stimuli to control cell growth, proliferation, and survival. The complexity of numerous intracellular signaling pathways is highlighted by the number of kinases encoded by the human genome (539) and the plethora of phosphorylation sites identified in phosphoproteomic studies. Perturbation of these signaling networks by mutations or abnormal protein expression underlies the cause of many diseases including cancer. Recent RNAi screens and cancer genomic sequencing studies have revealed that many more kinases than anticipated contribute to tumorigenesis and are potential targets for inhibitor drug development intervention. This review will highlight recent insights into known pathways essential for tumorigenesis and discuss exciting new pathways for therapeutic intervention.
dc.languageENG
dc.language.isoenen
dc.subjectCanceren
dc.subjectCell Signallingen
dc.titleProtein kinase signaling networks in cancer.en
dc.typeArticleen
dc.contributor.departmentSignalling Networks in Cancer Group, Cancer Research UK, Paterson Institute for Cancer Research, The University of Manchester, Manchester, UK.en
dc.identifier.journalCurrent Opinion in Genetics & Developmenten
html.description.abstractProtein kinases orchestrate the activation of signaling cascades in response to extracellular and intracellular stimuli to control cell growth, proliferation, and survival. The complexity of numerous intracellular signaling pathways is highlighted by the number of kinases encoded by the human genome (539) and the plethora of phosphorylation sites identified in phosphoproteomic studies. Perturbation of these signaling networks by mutations or abnormal protein expression underlies the cause of many diseases including cancer. Recent RNAi screens and cancer genomic sequencing studies have revealed that many more kinases than anticipated contribute to tumorigenesis and are potential targets for inhibitor drug development intervention. This review will highlight recent insights into known pathways essential for tumorigenesis and discuss exciting new pathways for therapeutic intervention.


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