Janus Kinases in Leukemia

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dc.contributor.author Raivola, Juuli
dc.contributor.author Haikarainen, Teemu
dc.contributor.author Abraham, Bobin George
dc.contributor.author Silvennoinen, Olli
dc.date.accessioned 2021-04-08T12:41:01Z
dc.date.available 2021-04-08T12:41:01Z
dc.date.issued 2021-02
dc.identifier.citation Raivola , J , Haikarainen , T , Abraham , B G & Silvennoinen , O 2021 , ' Janus Kinases in Leukemia ' , Cancers , vol. 13 , no. 4 , 800 . https://doi.org/10.3390/cancers13040800
dc.identifier.other PURE: 161905667
dc.identifier.other PURE UUID: a9cb9aeb-247e-4434-b705-bf1a3f7865d2
dc.identifier.other WOS: 000623344400001
dc.identifier.uri http://hdl.handle.net/10138/328842
dc.description.abstract Simple Summary Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway is a crucial cell signaling pathway that drives the development, differentiation, and function of immune cells and has an important role in blood cell formation. Mutations targeting this pathway can lead to overproduction of these cell types, giving rise to various hematological diseases. This review summarizes pathogenic JAK/STAT activation mechanisms and links known mutations and translocations to different leukemia. In addition, the review discusses the current therapeutic approaches used to inhibit constitutive, cytokine-independent activation of the pathway and the prospects of developing more specific potent JAK inhibitors. Janus kinases (JAKs) transduce signals from dozens of extracellular cytokines and function as critical regulators of cell growth, differentiation, gene expression, and immune responses. Deregulation of JAK/STAT signaling is a central component in several human diseases including various types of leukemia and other malignancies and autoimmune diseases. Different types of leukemia harbor genomic aberrations in all four JAKs (JAK1, JAK2, JAK3, and TYK2), most of which are activating somatic mutations and less frequently translocations resulting in constitutively active JAK fusion proteins. JAKs have become important therapeutic targets and currently, six JAK inhibitors have been approved by the FDA for the treatment of both autoimmune diseases and hematological malignancies. However, the efficacy of the current drugs is not optimal and the full potential of JAK modulators in leukemia is yet to be harnessed. This review discusses the deregulation of JAK-STAT signaling that underlie the pathogenesis of leukemia, i.e., mutations and other mechanisms causing hyperactive cytokine signaling, as well as JAK inhibitors used in clinic and under clinical development. en
dc.format.extent 20
dc.language.iso eng
dc.relation.ispartof Cancers
dc.rights cc_by
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject leukemia
dc.subject Janus kinases
dc.subject kinase inhibitor
dc.subject 3122 Cancers
dc.title Janus Kinases in Leukemia en
dc.type Review Article
dc.contributor.organization Helsinki Institute of Life Science HiLIFE
dc.contributor.organization Institute of Biotechnology
dc.contributor.organization University Management
dc.contributor.organization University of Helsinki
dc.description.reviewstatus Peer reviewed
dc.relation.doi https://doi.org/10.3390/cancers13040800
dc.relation.issn 2072-6694
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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