Abstract
Tumor metastasis can occur years after an apparent cure due to a phenomenon known as metastatic tumor dormancy; in which tumor masses or individual tumor cells are growth restricted for extended periods of time. This period of dormancy is induced and maintained by several mechanisms, including: (1) Tumor microenvironment factors such as cytokine expression, immunosurveillance and angiogenesis; (2) Metastasis suppressor gene activity; and (3) Cancer therapeutics. Disseminated tumor cells (DTC) are the key cells that result in dormant tumors. However, many challenges exist towards isolating DTCs for mechanistic studies. The main DTC that may represent the dormant cell is the cancer stem cells (CSC) as they have a slow proliferation rate. In addition to limited knowledge regarding induction of tumor dormancy, there are large gaps in knowledge regarding how tumors escape from dormancy. Emerging research into cancer stem cells, immunotherapy, and metastasis suppressor genes, may lead to new approaches for targeted anti-metastatic therapy to prevent dormancy escape. Overall, an enhanced understanding of tumor dormancy is critical for better targeting and treatment of patients to prevent cancer recurrence.
Highlights
The majority of cancer related deaths are due to metastatic outgrowths of the primary tumor mass that develop years to decades after apparent cures
There are multiple factors which contribute to tumor dormancy (Figure 1)
The microenvironment can inhibit the activation of angiogenesis, a necessary step for sustained metastatic growth
Summary
The majority of cancer related deaths are due to metastatic outgrowths of the primary tumor mass that develop years to decades after apparent cures. Metastatic spread of tumors is a well-coordinated sequence of events, where cells shed from primary tumors, enter blood circulation, and spread to distant organs [1,2]. This process is, highly inefficient, where the majority of cells are predicted to die upon dissemination. In addition to a proliferation-arrested state (G0/G1 arrest) clinical dormancy may be due to micro-metastases where active proliferation is counterbalanced by apoptosis [6] These metastatic growths are usually more malignant than the primary tumor, having acquired the ability to circumvent conventional therapies and growth barriers from non-permissive microenvironments
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