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Treatment-Induced Autophagy Associated with Tumor Dormancy and Relapse

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Technical Report,01 Jul 2016,30 Jun 2017

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Virginia Commonwealth University Richmond United States

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Studies relating to the role autophagy in tumor dormancy revealed that transient inhibition of autophagy during ADR treatment resulted in prolonging tumor dormancy. However, complete knockdown of autophagy gene expedited tumor relapse. The purpose of the study was to determine if transient blockade of autophagy by CQ was associated with antiinflammatory function of CQ independent of its role in autophagy. We showed that inhibition of tumorintrinsic inflammatory pathways, which was induced by ADR, prolonged tumor dormancy, in vitro and in vivo. Also, induction of tumorintrinsic inflammatory pathways reduced immune modulatory function of chemotherapy on dormant tumor cells, while increasing their susceptibility to antitumor T cell responses. These data suggests a paradoxical role for ADRinduced tumorintrinsic inflammatory pathways, facilitating tumor relapse on the one hand and increasing susceptibility of dormant tumor cells to immunotherapy on the other hand. Therefore, immunotherapy could be an option for preventing tumor relapse following chemotherapyinduced tumor dormancy.

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  • Medicine and Medical Research

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