Tumor Dormancy and Cancer Stem Cells: Two Sides of the Same Coin?
- 30 August 2012
- book chapter
- Published by Springer Science and Business Media LLC in Advances in Experimental Medicine and Biology
- Vol. 734, 145-179
- https://doi.org/10.1007/978-1-4614-1445-2_8
Abstract
Increasing evidence suggests that tumor dormancy represents an important mechanism underlying the observed failure of existing therapeutic modalities to fully eradicate cancers. In addition to its more established role in maintaining minimal residual disease after treatment, dormancy might also critically contribute to early stages of tumor development and the formation of clinically undetectable micrometastatic foci. There are striking parallels between the concept of tumor dormancy and the cancer stem cell (CSC) theory of tumor propagation. For instance, the CSC hypothesis similarly predicts that a subset of self-renewing cancer cells—that is CSCs—is responsible for tumor initiation, bears the preferential ability to survive tumor therapy, and persists long term to ultimately cause delayed cancer recurrence and metastatic progression. Additionally, many of the biological mechanisms involved in controlling the dormant state of a tumor can also govern CSC behavior, including cell cycle modifications, alteration of angiogenic processes, and modulation of antitumor immune responses. In fact, quiescence and immune escape are emerging hallmark features of at least some CSCs, indicating significant overlap between dormant cancer populations and CSCs. Herein, we crucially dissect whether CSCs occupy specific roles in orchestrating the switch between dormancy and exuberant tumor growth. We elucidate how recently uncovered CSC biological features could enable these cells to evade immunologic clearance and regulate cancer expansion, relapse, and progression. We propose that the study of CSC immunobiological pathways holds the promise to critically advance our understanding of the processes mediating tumor dormancy. Ultimately, such research endeavors could unravel novel therapeutic avenues that efficiently target both proliferating and dormant CSCs to minimize the risk of tumor recurrence in cancer patients.Keywords
This publication has 102 references indexed in Scilit:
- Phenotypic Heterogeneity among Tumorigenic Melanoma Cells from Patients that Is Reversible and Not Hierarchically OrganizedCancer Cell, 2010
- Epithelial-Mesenchymal Transitions in Development and DiseaseCell, 2009
- Identification and targeting of cancer stem cellsBioEssays, 2009
- Heterogeneity in Cancer: Cancer Stem Cells versus Clonal EvolutionCell, 2009
- CD47 Is an Adverse Prognostic Factor and Therapeutic Antibody Target on Human Acute Myeloid Leukemia Stem CellsCell, 2009
- Radiation responses of cancer stem cellsJournal of Cellular Biochemistry, 2009
- Hypoxia-Inducible Factors Regulate Tumorigenic Capacity of Glioma Stem CellsCancer Cell, 2009
- Systemic Spread Is an Early Step in Breast CancerCancer Cell, 2008
- Genomic analysis of single cytokeratin-positive cells from bone marrow reveals early mutational events in breast cancerCancer Cell, 2005
- Targeted disruption of β1-integrin in a transgenic mouse model of human breast cancer reveals an essential role in mammary tumor inductionCancer Cell, 2004