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dc.contributor.authorClapper, Erin
dc.contributor.authorDi Trapani, Giovanna
dc.contributor.authorTonissen, Kathryn F
dc.date.accessioned2020-12-04T00:03:07Z
dc.date.available2020-12-04T00:03:07Z
dc.date.issued2020
dc.identifier.issn1042-8194
dc.identifier.doi10.1080/10428194.2020.1849679
dc.identifier.urihttp://hdl.handle.net/10072/399938
dc.description.abstractChronic myeloid leukemia (CML) is usually characterized by the formation of the fusion onco-protein bcr-abl. Therefore, the majority of CML treatments are bcr-abl specific tyrosine kinase inhibitors (TKIs). TKI resistance in CML treatment is becoming a major obstacle in managing this disease. One well-studied form of drug resistance is hypoxia-induced drug resistance, a phenomenon observed in many other cancers. This study aimed to determine the efficacy of TKIs in CML cells cultured in hypoxia. It was observed that bcr-abl translation was severely halted in hypoxia, rendering TKIs ineffective. We found that the mechanism by which bcr-abl protein levels were being suppressed in hypoxia was through the mTOR pathway, specifically via ribosomal protein S6 (RPS6). This information is vital to the improvement of CML treatments, as it can be used to determine how to best combat hypoxia-induced drug resistance in CML and subsequently to identify new targets for treatment.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherInforma UK Limited
dc.relation.ispartofjournalLeukemia & Lymphoma
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchCardiovascular medicine and haematology
dc.subject.fieldofresearchcode3202
dc.subject.fieldofresearchcode3201
dc.titleThe regulation of bcr-abl in hypoxia is through the mTOR pathway
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationClapper, E; Di Trapani, G; Tonissen, KF, The regulation of bcr-abl in hypoxia is through the mTOR pathway, Leukemia & Lymphoma,
dc.date.updated2020-12-03T22:38:54Z
gro.description.notepublicThis publication has been entered as an advanced online version in Griffith Research Online.
gro.hasfulltextNo Full Text
gro.griffith.authorDi Trapani, Jenny
gro.griffith.authorTonissen, Kathryn F.


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