The findings presented by Kruer et al suggest a mechanism whereby, in the context of AZA-dependent XPO1 overexpression, the functional activity of p53 and transcription of its key downstream genes that have been restored by eprenetapopt are abolished via XPO1 (exportin-1)-mediated transport out of the nucleus, thus conferring resistance to the combination therapy. Treatment with XPO1 inhibitor is a proposed therapeutic approach for restoring nuclear p53 activity in combination with eprenetapopt. Figure created with BioRender.com. D’Andrea R. (2025) https://BioRender.com/te49jr2.

The findings presented by Kruer et al suggest a mechanism whereby, in the context of AZA-dependent XPO1 overexpression, the functional activity of p53 and transcription of its key downstream genes that have been restored by eprenetapopt are abolished via XPO1 (exportin-1)-mediated transport out of the nucleus, thus conferring resistance to the combination therapy. Treatment with XPO1 inhibitor is a proposed therapeutic approach for restoring nuclear p53 activity in combination with eprenetapopt. Figure created with BioRender.com. D’Andrea R. (2025) https://BioRender.com/te49jr2.

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