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dc.contributor.authorVandenberg, CJ
dc.contributor.authorMotoyama, N
dc.contributor.authorCory, S
dc.date.accessioned2020-12-22T05:23:41Z
dc.date.available2020-12-22T05:23:41Z
dc.date.issued2016-01-01
dc.identifierpii: cddis2015396
dc.identifier.citationVandenberg, C. J., Motoyama, N. & Cory, S. (2016). FoxO3 suppresses Myc-driven lymphomagenesis. CELL DEATH & DISEASE, 7 (1), https://doi.org/10.1038/cddis.2015.396.
dc.identifier.issn2041-4889
dc.identifier.urihttp://hdl.handle.net/11343/258278
dc.description.abstractThis study demonstrates, for the first time, that loss of a single forkhead box class O (FoxO) transcription factor, can promote lymphomagenesis. Using two different mouse models, we show that FoxO3 has a significant tumour-suppressor function in the context of Myc-driven lymphomagenesis. Loss of FoxO3 significantly accelerated myeloid tumorigenesis in vavP-MYC10 transgenic mice and B lymphomagenesis in Eμ-myc transgenic mice. Tumour analysis indicated that the selective pressure for mutation of the p53 pathway during Eμ-myc lymphomagenesis was not altered. Frank tumours were preceded by elevated macrophage numbers in FoxO3(-/-) vavP-MYC10 mice but, surprisingly, pre-B-cell numbers were relatively normal in healthy young FoxO3(-/-)Eμ-myc mice. In vitro assays revealed enhanced survival capacity of Myc-driven cells lacking FoxO3, but no change in cell cycling was detected. The loss of FoxO3 may also be affecting other tumour-suppressive functions for which FoxO1/4 cannot fully compensate.
dc.languageEnglish
dc.publisherNATURE PUBLISHING GROUP
dc.titleFoxO3 suppresses Myc-driven lymphomagenesis
dc.typeJournal Article
dc.identifier.doi10.1038/cddis.2015.396
melbourne.affiliation.departmentMedical Biology (W.E.H.I.)
melbourne.source.titleCell Death and Disease
melbourne.source.volume7
melbourne.source.issue1
dc.rights.licenseCC BY
melbourne.elementsid1037453
melbourne.openaccess.pmchttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816178
melbourne.contributor.authorVandenberg, Cassandra
melbourne.contributor.authorCory, Suzanne
dc.identifier.eissn2041-4889
melbourne.accessrightsOpen Access


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