Cytogenetics and molecular genetics

Fusion of the CRM1 nuclear export receptor to AF10 causes leukemia and transcriptional activation of HOXA genes

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Fig. 1: CRM1-AF10 and CRM1Δ-AF10 display leukemogenic activity.
Fig. 2: Impairing the NUP214/CRM1 interaction abrogates leukemia development.


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CRM1 plasmids containing mutants in the NUP214 binding region were generously provided by Ralph Kehlenbach and Sarah Port. Pritha Bagchi, PhD and the Emory Integrated Proteomics Core provided assistance with BioID2 Mass Spectrometry. This work was supported by an American Society of Hematology Research Training Award for Fellows (WKA), Hyundai Hope on Wheels Young Investigator Award (WKA and CPL), Hyundai Hope On Wheels Scholar Award (CPL and DSW), the Duke Cancer Institute (CPL), a NIH R03 grant (1R03CA191983-01A1, CPL), Alex’s Lemonade Stand Young Investigator Award (JLH), Pablove Foundation (JLH), Pediatric Cancer Research Foundation (JLH), NHLBI T32 5T32HL007057-37 (WKA), NHLBI T32 5T32HL007057-40 (SKS), a St. Baldrick’s Foundation Research Award (DSW), and the Schiffman Family Foundation. CPL is an INSERM scientist.

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Correspondence to Daniel S. Wechsler or Catherine P. Lavau.

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None of the authors has any direct or indirect commercial financial incentive associated with publishing this article. None of the authors has an affiliation with any organization that, to our knowledge, has a direct interest in the subject matter discussed. The Wechsler Laboratory received financial support from Karyopharm, Inc. several years prior to performing the work described in this manuscript, but no Karyopharm products were used for the studies described here.

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Aumann, W.K., Heath, J.L., Conway, A.E. et al. Fusion of the CRM1 nuclear export receptor to AF10 causes leukemia and transcriptional activation of HOXA genes. Leukemia (2020).

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