This review explores genetic and receptor interactions influencing breast cancer dormancy, suggesting therapeutic strategies.
Late recurrence of breast cancer poses a considerable threat to patient survival, often attributed to breast cancer dormancy. Dormancy, characterized by cancer cells remaining quiescent for extended periods, is influenced by genetic factors and modifications that directly impact cellular phenotype. Alterations in gene expression dynamically shape cellular behavior, often mediated through receptor signaling pathways. Moreover, interactions within the tumor microenvironment play a pivotal role, fostering either cancer cell dormancy or promoting their escape from dormancy. This review endeavors to provide a comprehensive synthesis of recent advancements in understanding breast cancer dormancy across genetic, receptor molecular, and cellular dimensions. By elucidating the intricate mechanisms underlying dormancy, we aim to shed light on potential therapeutic strategies to prevent late recurrences. Furthermore, we anticipate future research directions that may uncover novel insights into this complex phenomenon, ultimately improving patient outcomes and refining clinical management strategies for breast cancer recurrence.
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Ma et al. (2025) studied this question.
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