This study was conducted in order to understand Treatment-persistent residual tumors impede curative cancer therapy. 3D organoid cultures simulate the emergence of treatment-persistent residual tumors. Treatment-persistent tumor cells in organoids, xenografts, and cancer patients adopt a distinct and reversible transcriptional program resembling that of embryonic diapause, a dormant stage of suspended development triggered by stress and associated with suppressed Myc activity and overall biosynthesis. Myc-suppressed cancer cells survive via reduced redox stress and apoptotic priming. This study demonstrates that cancer co-opts a mechanism similar to diapause with adaptive inactivation of Myc to persist during treatment. CDK9 inhibition reverts biosynthetic pause and enhances chemosensitivity.

 As a conclusion we can say that, maintaining residual cells in dormancy after chemotherapy by inhibiting Myc activity or interfering with the diapause-like adaptation by inhibiting cyclin-dependent kinase 9 represent potential therapeutic strategies against chemotherapy-persistent tumor cells. Chemo-persister cells have suppressed Myc and a diapause-like molecular adaptation. An Embryonic Diapause-like Adaptation with Suppressed Myc Activity Enables Tumor Treatment Persistence. 

Reference- https://www.cell.com/cancer-cell/fulltext/S1535-6108(20)30609-7 

Author