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dc.contributor.authorNewton, A
dc.contributor.authorBrognard, John
dc.date.accessioned2017-04-19T16:43:27Z
dc.date.available2017-04-19T16:43:27Z
dc.date.issued2017-03-07
dc.identifier.citationReversing the paradigm: protein kinase C as a tumor suppressor. 2017, Trends Pharmacol Scien
dc.identifier.issn1873-3735
dc.identifier.pmid28283201
dc.identifier.doi10.1016/j.tips.2017.02.002
dc.identifier.urihttp://hdl.handle.net/10541/620252
dc.description.abstractThe discovery in the 1980s that protein kinase C (PKC) is a receptor for the tumor-promoting phorbol esters fueled the dogma that PKC is an oncoprotein. Yet 30+ years of clinical trials for cancer using PKC inhibitors not only failed, but in some instances worsened patient outcome. The recent analysis of cancer-associated mutations, from diverse cancers and throughout the PKC family, revealed that PKC isozymes are generally inactivated in cancer, supporting a tumor suppressive function. In keeping with a bona fide tumor suppressive role, germline causal loss-of-function (LOF) mutations in one isozyme have recently been identified in lymphoproliferative disorders. Thus, strategies in cancer treatment should focus on restoring rather than inhibiting PKC.
dc.language.isoenen
dc.rightsArchived with thanks to Trends in pharmacological sciencesen
dc.titleReversing the paradigm: protein kinase C as a tumor suppressor.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pharmacology, University of California, San Diego, La Jolla, CA 92093-0721, USAen
dc.identifier.journalTrends in Pharmacological Sciencesen
html.description.abstractThe discovery in the 1980s that protein kinase C (PKC) is a receptor for the tumor-promoting phorbol esters fueled the dogma that PKC is an oncoprotein. Yet 30+ years of clinical trials for cancer using PKC inhibitors not only failed, but in some instances worsened patient outcome. The recent analysis of cancer-associated mutations, from diverse cancers and throughout the PKC family, revealed that PKC isozymes are generally inactivated in cancer, supporting a tumor suppressive function. In keeping with a bona fide tumor suppressive role, germline causal loss-of-function (LOF) mutations in one isozyme have recently been identified in lymphoproliferative disorders. Thus, strategies in cancer treatment should focus on restoring rather than inhibiting PKC.


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