Discovery of the cancer stem cell related determinants of radioresistance
Research output: Contribution to journal › Review article › Invited › peer-review
Contributors
Abstract
Tumors are known to be heterogeneous containing a dynamic mixture of phenotypically and functionally different tumor cells. The two concepts attempting to explain the origin of intratumor heterogeneity are the cancer stem cell hypothesis and the clonal evolution model. The stochastic model argues that tumors are biologically homogenous and all cancer cells within the tumor have equal ability to propagate the tumor growth depending on continuing mutations and selective pressure. By contrast, the stem cells model suggests that cancer heterogeneity is due to the hierarchy that originates from a small population of cancer stem cells (CSCs) which are biologically distinct from the bulk tumor and possesses self-renewal, tumorigenic and multilineage potential. Although these two hypotheses have been discussed for a long time as mutually exclusive explanations of tumor heterogeneity, they are easily reconciled serving as a driving force of cancer evolution and diversity. Recent discovery of the cancer cell plasticity and heterogeneity makes the CSC population a moving target that could be hard to track and eradicate. Understanding the signaling mechanisms regulating CSCs during the course of cancer treatment can be indispensable for the optimization of current treatment strategies.
Details
Original language | English |
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Pages (from-to) | 378-387 |
Number of pages | 10 |
Journal | Radiotherapy and Oncology |
Volume | 108 |
Issue number | 3 |
Publication status | Published - Sept 2013 |
Peer-reviewed | Yes |
External IDs
Scopus | 84887019122 |
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PubMed | 23830195 |
ORCID | /0000-0002-5247-908X/work/142241913 |
Keywords
Sustainable Development Goals
Keywords
- Animals, High-Throughput Screening Assays, Humans, Neoplasms/radiotherapy, Neoplastic Stem Cells/radiation effects, Radiation Tolerance, Tumor Microenvironment