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               <mods:identifier type="citation">FEBS Lett. 2016 Jul;590(14):2063-75.</mods:identifier>
               <mods:identifier type="doi">10.1002/1873-3468.12243</mods:identifier>
               <mods:identifier type="e-issn">1873-3468</mods:identifier>
               <mods:identifier type="journal">FEBS Letters</mods:identifier>
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               <mods:identifier type="uri">http://hdl.handle.net/20.500.12105/13225</mods:identifier>
               <mods:abstract>Ewing sarcoma (ES) is an aggressive pediatric tumor driven by the fusion protein EWS-FLI1. We report that EWS-FLI1 suppresses TDO2-mediated tryptophan (TRP) breakdown in ES cells. Gene expression and metabolite analyses reveal an EWS-FLI1-dependent regulation of TRP metabolism. TRP consumption increased in the absence of EWS-FLI1, resulting in kynurenine and kynurenic acid accumulation, both aryl hydrocarbon receptor (AHR) ligands. Activated AHR binds to the promoter region of target genes. We demonstrate that EWS-FLI1 knockdown results in AHR nuclear translocation and activation. Our data suggest that EWS-FLI1 suppresses autocrine AHR signaling by inhibiting TDO2-catalyzed TRP breakdown.</mods:abstract>
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                  <mods:topic>EWS-FLI1</mods:topic>
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                  <mods:topic>Tryptophan</mods:topic>
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                  <mods:title>EWS-FLI1 impairs aryl hydrocarbon receptor activation by blocking tryptophan breakdown via the kynurenine pathway</mods:title>
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