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dc.contributor.authorKeane, N A
dc.contributor.authorReidy, M
dc.contributor.authorNatoni, A
dc.contributor.authorRaab, M S
dc.contributor.authorO'Dwyer, M
dc.date.accessioned2017-03-07T09:50:10Z
dc.date.available2017-03-07T09:50:10Z
dc.date.issued2015-07-17
dc.identifier.citationTargeting the Pim kinases in multiple myeloma. 2015, 5:e325 Blood Cancer Jen
dc.identifier.issn2044-5385
dc.identifier.pmid26186558
dc.identifier.doi10.1038/bcj.2015.46
dc.identifier.urihttp://hdl.handle.net/10147/621140
dc.description.abstractMultiple myeloma (MM) is a plasma cell malignancy that remains incurable. Novel treatment strategies to improve survival are urgently required. The Pims are a small family of serine/threonine kinases with increased expression across the hematological malignancies. Pim-2 shows highest expression in MM and constitutes a promising therapeutic target. It is upregulated by the bone marrow microenvironment to mediate proliferation and promote MM survival. Pim-2 also has a key role in the bone destruction typically seen in MM. Additional putative roles of the Pim kinases in MM include trafficking of malignant cells, promoting oncogenic signaling in the hypoxic bone marrow microenvironment and mediating resistance to therapy. A number of Pim inhibitors are now under development with lead compounds entering the clinic. The ATP-competitive Pim inhibitor LGH447 has recently been reported to have single agent activity in MM. It is anticipated that Pim inhibition will be of clinical benefit in combination with standard treatments and/or with novel drugs targeting other survival pathways in MM.
dc.language.isoenen
dc.publisherNature Publishing Groupen
dc.rightsArchived with thanks to Blood cancer journalen
dc.subjectCANCERen
dc.subjectMULTIPLE MYELOMAen
dc.subject.meshAnimals
dc.subject.meshAntineoplastic Agents
dc.subject.meshCell Proliferation
dc.subject.meshDrug Resistance, Neoplasm
dc.subject.meshGene Expression Regulation, Neoplastic
dc.subject.meshHumans
dc.subject.meshMolecular Targeted Therapy
dc.subject.meshMultiple Myeloma
dc.subject.meshProtein Kinase Inhibitors
dc.subject.meshProto-Oncogene Proteins c-pim-1
dc.subject.meshSignal Transduction
dc.subject.meshUp-Regulation
dc.titleTargeting the Pim kinases in multiple myeloma.en
dc.typeArticleen
dc.identifier.journalBlood cancer journalen
dc.description.fundingOtheren
dc.description.provinceConnachten
dc.description.peer-reviewpeer-reviewen
refterms.dateFOA2018-08-27T19:53:18Z
html.description.abstractMultiple myeloma (MM) is a plasma cell malignancy that remains incurable. Novel treatment strategies to improve survival are urgently required. The Pims are a small family of serine/threonine kinases with increased expression across the hematological malignancies. Pim-2 shows highest expression in MM and constitutes a promising therapeutic target. It is upregulated by the bone marrow microenvironment to mediate proliferation and promote MM survival. Pim-2 also has a key role in the bone destruction typically seen in MM. Additional putative roles of the Pim kinases in MM include trafficking of malignant cells, promoting oncogenic signaling in the hypoxic bone marrow microenvironment and mediating resistance to therapy. A number of Pim inhibitors are now under development with lead compounds entering the clinic. The ATP-competitive Pim inhibitor LGH447 has recently been reported to have single agent activity in MM. It is anticipated that Pim inhibition will be of clinical benefit in combination with standard treatments and/or with novel drugs targeting other survival pathways in MM.


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