Targeting Dormant Tumor Cells: A Promising Strategy to Prevent Breast Cancer Recurrence

Breast cancer recurrence is often driven by dormant disseminated tumor cells (DTCs) persisting in bone marrow and other niches.
Preclinical mouse models identified autophagy and mTOR signaling as key regulators of tumor cell dormancy and reactivation.
Inhibition of autophagy with hydroxychloroquine (HCQ) and mTOR signaling with everolimus (EVE) decreased residual tumor cell burden and improved recurrence-free survival (RFS) in a duration-dependent manner.
The CLEVER phase 2 trial demonstrated that targeting dormant DTCs with HCQ, EVE, or their combination is safe, feasible, and leads to significant reductions or clearance of DTCs in breast cancer survivors within 5 years of diagnosis.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Breast cancer recurrence is often driven by dormant disseminated tumor cells (DTCs) persisting in bone marrow and other niches.
Preclinical mouse models identified autophagy and mTOR signaling as key regulators of tumor cell dormancy and reactivation.
Inhibition of autophagy with hydroxychloroquine (HCQ) and mTOR signaling with everolimus (EVE) decreased residual tumor cell burden and improved recurrence-free survival (RFS) in a duration-dependent manner.
The CLEVER phase 2 trial demonstrated that targeting dormant DTCs with HCQ, EVE, or their combination is safe, feasible, and leads to significant reductions or clearance of DTCs in breast cancer survivors within 5 years of diagnosis.

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