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      Liquid biopsy for monitoring of tumor dormancy and early detection of disease recurrence in solid tumors

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          Abstract

          Cancer is one of the three leading causes of death worldwide. Even after successful therapy and achieving remission, the risk of relapse often remains. In this context, dormant residual cancer cells in secondary organs such as the bone marrow constitute the cellular reservoir from which late tumor recurrences arise. This dilemma leads the term of minimal residual disease, which reflects the presence of tumor cells disseminated from the primary lesion to distant organs in patients who lack any clinical or radiological signs of metastasis or residual tumor cells left behind after therapy that eventually lead to local recurrence. Disseminated tumor cells have the ability to survive in a dormant state following treatment and linger unrecognized for more than a decade before emerging as recurrent disease. They are able to breakup their dormant state and to readopt their proliferation under certain circumstances, which can finally lead to distant relapse and cancer-associated death. In recent years, extensive molecular and genetic characterization of disseminated tumor cells and blood-based biomarker has contributed significantly to our understanding of the frequency and prevalence of tumor dormancy. In this article, we describe the clinical relevance of disseminated tumor cells and highlight how latest advances in different liquid biopsy approaches can be used to detect, characterize, and monitor minimal residual disease in breast cancer, prostate cancer, and melanoma patients.

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          The senescence-associated secretory phenotype: the dark side of tumor suppression.

          Cellular senescence is a tumor-suppressive mechanism that permanently arrests cells at risk for malignant transformation. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.
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            A perspective on cancer cell metastasis.

            Metastasis causes most cancer deaths, yet this process remains one of the most enigmatic aspects of the disease. Building on new mechanistic insights emerging from recent research, we offer our perspective on the metastatic process and reflect on possible paths of future exploration. We suggest that metastasis can be portrayed as a two-phase process: The first phase involves the physical translocation of a cancer cell to a distant organ, whereas the second encompasses the ability of the cancer cell to develop into a metastatic lesion at that distant site. Although much remains to be learned about the second phase, we feel that an understanding of the first phase is now within sight, due in part to a better understanding of how cancer cell behavior can be modified by a cell-biological program called the epithelial-to-mesenchymal transition.
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              Cancer immunoediting: from immunosurveillance to tumor escape.

              The concept that the immune system can recognize and destroy nascent transformed cells was originally embodied in the cancer immunosurveillance hypothesis of Burnet and Thomas. This hypothesis was abandoned shortly afterwards because of the absence of strong experimental evidence supporting the concept. New data, however, clearly show the existence of cancer immunosurveillance and also indicate that it may function as a component of a more general process of cancer immunoediting. This process is responsible for both eliminating tumors and sculpting the immunogenic phenotypes of tumors that eventually form in immunocompetent hosts. In this review, we will summarize the historical and experimental basis of cancer immunoediting and discuss its dual roles in promoting host protection against cancer and facilitating tumor escape from immune destruction.
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                Author and article information

                Contributors
                pantel@uke.de
                Journal
                Cancer Metastasis Rev
                Cancer Metastasis Rev
                Cancer Metastasis Reviews
                Springer US (New York )
                0167-7659
                1573-7233
                6 January 2023
                6 January 2023
                2023
                : 42
                : 1
                : 161-182
                Affiliations
                [1 ]GRID grid.412315.0, Institute for Tumor Biology, , University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, ; Martinistr. 52, 20246 Hamburg, Germany
                [2 ]GRID grid.13648.38, ISNI 0000 0001 2180 3484, Skin Cancer Center, Department of Dermatology and Venereology, , University Hospital Hamburg-Eppendorf, ; Hamburg, Germany
                [3 ]GRID grid.412315.0, Mildred-Scheel-Nachwuchszentrum HaTRiCs4, Universitäres Cancer Center Hamburg, ; Hamburg, Germany
                Article
                10075
                10.1007/s10555-022-10075-x
                10014694
                36607507
                c9605f4c-e01d-40f0-b1f0-bcf051eafa55
                © The Author(s) 2023

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 2 September 2022
                : 22 December 2022
                Funding
                Funded by: Universitätsklinikum Hamburg-Eppendorf (UKE) (5411)
                Categories
                Article
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2023

                Oncology & Radiotherapy
                minimal residual disease,disseminated tumor cells,circulating tumor cells,circulating tumor dna,breast cancer,prostate cancer,melanoma

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