Introduction to the Special Issue “Cancer Stem Cells: Impact on Treatment”
Laboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Department of Therapeutic Radiology and Oncology, Innsbruck Medical University, 6020 Innsbruck, Austria.
Correspondence Address: Dr. Ira-Ida Skvortsova, Laboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Department of Therapeutic Radiology and Oncology, Innsbruck Medical University, 6020 Innsbruck, Austria. E-mail:
Despite the fact that currently existing therapeutic approaches are highly effective and can markedly improve clinical outcome in cancer patients with even advanced diseases, the problems of treatment resistance, therapy recurrences and unfavorable disease progression are still not solved. It is generally believed that the small population of the intratumoral carcinoma stem cells (CSCs) is responsible for poor clinical outcome, because CSCs are considered as a reason for the tumor heterogeneity, diminished sensitivity to chemo- and radiotherapy and enhanced abilities for metastatic spread.[1-5] Investigation of the biological properties of CSCs is a hot topic in cancer research. In order to know more about CSC behavior, it is necessary to possess the CSC-specific molecular patterns distinguishing CSCs from non-CSCs. Using currently existing surrogate CSC biomarkers [CD133 (prominin-1), CD44, CD24, Bmi-1, Notch family members, Hedgehog, aldehyde dehydrogenase 1 (ALDH1), nestin, etc.], subpopulations carcinoma cells with stem cell properties can be isolated for further investigations. Recent studies have demonstrated that a variety of intracellular pathways are affected in CSCs: CSC metabolism is characterized by activation of glycolytic pathways and intracellular redox potential is dysregulated;[1,7,8] molecular mechanisms governing cell cycle, cell proliferation and cell death development are also disrupted. Thus, there is a hypothesis that one of the reasons of CSC insensitivity to chemotherapeutics and ionizing radiation is the slower CSC proliferation and CSC quiescence. It is known that chemotherapeutic agents and radiotherapy eradicate fast dividing and proliferating carcinoma cells more effectively than the slower dividing cells. Therefore, it is logical to suggest that quiescent CSCs should be changed in their intracellular signalings underlying cell cycle regulation and cell division. Indeed, Gardane et al. and Vaidya in their article have clearly demonstrated that low doses of curcumin can accelerate proliferation of the leukemic cells and application of 5-fluorouracil becomes more effective compared to the treatment with 5-fluorouracil without curcumin. These findings help to assume that administration of the compounds affecting quiescence of carcinoma cells can improve therapy results in cancer patients with malignant tumors containing a high number of quiescent CSCs.
Review article by Kim et al. highlights therapeutic opportunities to target CSCs and to reach better treatment results in cancer patients. Recent years have seen an increased number of research reports on the CSC-related intracellular and intratumoral molecular pathways that can be effectively blocked in order to reach better survival rate in cancer patients. This review article provides an analysis of different strategies that can be introduced into the clinical practice in order to improve therapy outcome in patients with unfavourable prognosis.
The Guest Editor and contributors to this special issue of the journal Journal of Cancer Metastasis and Treatment hope that basic researchers and clinicians will read these articles with great interest.
I am heartily thankful and owe my deepest gratitude to Dandan Yu and Lisa Huang for their boundless readiness to help and assist during processing of the submitted articles and in the preparation of this issue.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
1. Skvortsova I, Debbage P, Kumar V, Skvortsov S. Radiation resistance: cancer stem cells (CSCs) and their enigmatic pro-survival signaling. Semin Cancer Biol 2015;35:39-44.
2. Skvortsov S, Debbage P, Skvortsova I. Proteomics of cancer stem cells. Int J Radiat Biol 2014;90:653-8.
3. Skvortsov S, Debbage P, Lukas P, Skvortsova I. Crosstalk between DNA repair and cancer stem cell (CSC) associated intracellular pathways. Semin Cancer Biol 2015;31:36-42.
5. Dingli D, Michor F. Successful therapy must eradicate cancer stem cells. Stem Cells 2006;24:2603-10.
6. Margineantu DH, Hockenbery DM. Mitochondrial functions in stem cells. Curr Opin Genet Dev 2016;38:110-7.
7. Vlashi E, Lagadec C, Vergnes L, Matsutani T, Masui K, Poulou M, Popescu R, Della Donna L, Evers P, Dekmezian C, Reue K, Christofk H, Mischel PS, Pajonk F. Metabolic state of glioma stem cells and nontumorigenic cells. Proc Natl Acad Sci U S A 2011;108:16062-7.
8. Lagadec C, Dekmezian C, Bauché L, Pajonk F. Oxygen levels do not determine radiation survival of breast cancer stem cells. PLoS One 2012;7:e34545.
9. Gardane A, Poonawala M, Vaidya A. Curcumin sensitizes quiescent leukemic cells to anti-mitotic drug 5-fluorouracil by inducing proliferative responses in them. J Cancer Metasta Treat 2016;2:245-52.
10. Vaidya A. The quintessential quiescence of cancer stem cells: a struggle towards better treatment. J Cancer Metasta Treat 2016;2:243-4.
Cite This Article
Skvortsova II. Introduction to the Special Issue “Cancer Stem Cells: Impact on Treatment”. J Cancer Metastasis Treat 2016;2:231-2. http://dx.doi.org/10.20517/2394-4722.2016.35
Skvortsova II. Introduction to the Special Issue “Cancer Stem Cells: Impact on Treatment”. Journal of Cancer Metastasis and Treatment. 2016; 2: 231-2. http://dx.doi.org/10.20517/2394-4722.2016.35
Skvortsova, Ira-Ida. 2016. "Introduction to the Special Issue “Cancer Stem Cells: Impact on Treatment”" Journal of Cancer Metastasis and Treatment. 2: 231-2. http://dx.doi.org/10.20517/2394-4722.2016.35
Skvortsova, I.I. Introduction to the Special Issue “Cancer Stem Cells: Impact on Treatment”. J. Cancer. Metastasis. Treat. 2016, 2, 231-2. http://dx.doi.org/10.20517/2394-4722.2016.35
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