Abstract
In past decades, cancer patient survival has been improved with earlier detection and advancements in therapy. However, many patients who exhibit no clinical symptoms after frontline therapy subsequently suffer, often many years later, aggressive tumor recurrence. Cancer recurrence represents a critical clinical challenge in effectively treating malignancies and for patients’ quality of life. Tumor cell dormancy may help to explain treatment resistance and recurrence or metastatic reactivation. Understanding the dormant stage of tumor cells may help in discovering ways to maintain the dormant state or permanently eliminate dormant residual disseminated tumor cells. Over the past decade, numerous studies indicate that various mechanisms of tumor dormancy exist, including cellular dormancy (quiescence), angiogenic dormancy, and immunologic dormancy. In this short review, we summarize recent experimental and clinical evidence for these three mechanisms and other possible tumor microenvironment mechanisms that may influence tumor dormancy.
Highlights
Tumor dormancy is a recognized clinical phenomenon in which disseminated tumor cells (DTCs) remain occult, asymptomatic, and undetectable over a prolonged period of time
Tumor dormancy may contribute to tumor progression and relapse, either locally or metastatically at distant sites, years or decades after treatment
Clinical dormancy is frequently observed in many types of tumors, such as breast cancer (BC) [1], prostate cancer (PC) [2,3], melanoma [4,5], and B-cell lymphoma [6,7]
Summary
Tumor dormancy is a recognized clinical phenomenon in which disseminated tumor cells (DTCs) remain occult, asymptomatic, and undetectable over a prolonged period of time. Numerous immune cell types may enhance indirect escape from dormancy through their infiltration into the tumor microenvironment; these cell types include myeloid-derived suppressor cells, regulatory T-cells, and tumor-associated macrophages [27,42,43] These cells can secret numerous mitogens, cytokines, and some angiogenic factors to promote angiogenesis, cell proliferation, and immunosuppression [40]. As DNA damage accumulates in DTCs following cancer treatment, NHEJ may be upregulated to repair these damages and allow tumor cells to survive; this pathway creates genomic instability in the tumor cells In certain microenvironments, these genomically unstable DTCs may become dormant, maintain dormancy, or eventually reactivate, becoming more aggressive and leading to cancer recurrence. This idea needs to be tested in vitro and in vivo with an appropriate dormancy model
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