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dc.contributor.authorPabla, Navjotsingh
dc.contributor.authorDong, Zheng
dc.date.accessioned2012-10-26T16:29:36Z
dc.date.available2012-10-26T16:29:36Z
dc.date.issued2012-01-31en_US
dc.identifier.citationOncotarget. 2012 Jan 31; 3(1):107-111en_US
dc.identifier.issn1949-2553en_US
dc.identifier.pmid22403741en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/698
dc.description.abstractThe efficacy of chemotherapy is often limited by side effects in normal tissues. This is exemplified by cisplatin, a widely used anti-cancer drug that may induce serious toxicity in normal tissues and organs including the kidneys. Decades of research have delineated multiple signaling pathways that lead to kidney cell injury and death during cisplatin treatment. However, the same signaling pathways may also be activated in cancer cells and be responsible for the chemotherapeutic effects of cisplatin in tumors and, as a result, blockade of these pathways is expected to reduce the side effects as well as the anti-cancer efficacy. Thus, to effectively curtail the side effects, it is imperative to elucidate and target the cell killing mechanisms that are specific to normal (and not cancer) tissues. Our recent work identified protein kinase C δ (PKCδ) as a new and critical mediator of cisplatin-induced kidney cell injury and death. Importantly, inhibition of PKCδ enhanced the chemotherapeutic effects of cisplatin in several tumor models while alleviating the side effect in kidneys, opening a new avenue for normal tissue protection during chemotherapy.
dc.rightsCopyright: © 2012 Pabla and Dongen_US
dc.subjectResearch Perspectivesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntineoplastic Combined Chemotherapy Protocolsen_US
dc.subject.meshCisplatinen_US
dc.subject.meshCytoprotectionen_US
dc.subject.meshDrug Toxicityen_US
dc.subject.meshHumansen_US
dc.subject.meshKidney Diseasesen_US
dc.subject.meshNeoplasmsen_US
dc.subject.meshProtein Kinase C-deltaen_US
dc.subject.meshSignal Transductionen_US
dc.titleCurtailing side effects in chemotherapy: a tale of PKCδ in cisplatin treatmenten_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3292897en_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomy
refterms.dateFOA2019-04-10T00:33:57Z
html.description.abstractThe efficacy of chemotherapy is often limited by side effects in normal tissues. This is exemplified by cisplatin, a widely used anti-cancer drug that may induce serious toxicity in normal tissues and organs including the kidneys. Decades of research have delineated multiple signaling pathways that lead to kidney cell injury and death during cisplatin treatment. However, the same signaling pathways may also be activated in cancer cells and be responsible for the chemotherapeutic effects of cisplatin in tumors and, as a result, blockade of these pathways is expected to reduce the side effects as well as the anti-cancer efficacy. Thus, to effectively curtail the side effects, it is imperative to elucidate and target the cell killing mechanisms that are specific to normal (and not cancer) tissues. Our recent work identified protein kinase C δ (PKCδ) as a new and critical mediator of cisplatin-induced kidney cell injury and death. Importantly, inhibition of PKCδ enhanced the chemotherapeutic effects of cisplatin in several tumor models while alleviating the side effect in kidneys, opening a new avenue for normal tissue protection during chemotherapy.


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