Cancer Stem Cells as a new promising approach of efficient oncological treatment - the review of literature
KeywordsCancer stem cells, elective treatment, chemotherapy, remission
Introduction and purpose:
For many years a lot of research projects have been conducted with the aim to discover special cells, which are responsible for a neoplasm development. One of the theories concerns cancer stem cells (CSCs). This theory presumes the existence of original, undifferentiated cancer cells. These cells are capable of transform to all types of cells in neoplasm mass. The purpose of this study was to review the currently available data about the theory of CSCs and especially potential usage of this theory in oncological treatment. Pubmed and Scopus databases from the last 10 years were searched for phrase “cancer stem cells”.
A brief description of the state of knowledge:
Impaired signalling pathways lead to an occurrence of CSCs which may contribute to the development of neoplasm eventually. It is proved, that gamma secretase inhibitors impede Notch signalling pathway, which leads to a decrease of tumour markers expression and consequently decline in vivo tumour growth. It is believed that epigenetic mechanisms, including DNA methylation, histones alteration and RNA orientation are pivotal regulators of CSCs. It was shown, that histone deacetylases (HDAC) modulate refractoriness on chemotherapy in haematological tumours. It is also evidenced that peculiar designed microRNA directly inhibit CD44 which suppresses prostatic cancer stem cells and its metastases. CSCs have high expression of programmed death-ligand 1 (PD-L1) including breast and colon cancer, which proclaims in favour of immunotherapy aimed on CSCs.
Constantly growing knowledge about CSCs biology is creating new opportunities of detection, isolation and design of the therapies aimed on CSCs.
IARC. Global Cancer Observatory (GLOBOCAN) Cancer Tomorrow 2018 Estimates. Available at: http://gco.iarc.fr/tomorrow.
Badowska-Kozakiewicz AM, Budzik MP. Cancer stem cells – a new chance for successful treatment of cancer. Studia Medyczne 2015; 31 (2): 139–145.
Wieczorek K, Niewiarowska J. Cancer stem cells. Postepy Hig Med Dosw. 2012; 66: 629-636.
Nassar D, Blanpain C. Cancer Stem Cells: Basic Concepts and Therapeutic Implications. Annu Rev Pathol. 2016; 11: 47-76.
Turdo A, Veschi V, Gaggianesi M, Chinnici A, Bianca P, Todaro M et al.Meeting the Challenge of Targeting Cancer Stem Cells. Front Cell Dev Biol. 2019; 7: 16.
Szaryńska M, Olejniczak A, Kmieć Z. The role of cancer stem cells in pathogenesis of colorectal cancer. Postepy Hig Med Dosw. 2016; 70: 1469-1482.
Toh TB, Lim JJ, Chow EK. Epigenetics in cancer stem cells. Mol Cancer. 2017; 16(1): 29.
Zhang B, Strauss AC, Chu S, Li M, Ho Y, Shiang KD et al. Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate. Cancer Cell. 2010; 17(5): 427-42.
Li L, Wang L, Li L, Wang Z, Ho Y, McDonald T et al. Activation of p53 by SIRT1 inhibition enhances elimination of CML leukemia stem cells in combination with imatinib. Cancer Cell. 2012; 21(2): 266-81.
Liu C, Kelnar K, Liu B, Chen X, Calhoun-Davis T, Li H et al. The microRNA miR-34a inhibits prostate cancer stem cells and metastasis by directly repressing CD44. Nat Med. 2011; 17(2): 211-5.
Dawood S, Austin L, Cristofanilli M. Cancer stem cells: implications for cancer therapy. Oncology (Williston Park). 2014; 28(12): 1101-7, 1110.
Pan E, Supko JG, Kaley TJ, Butowski NA, Cloughesy T, Jung J et al. Phase I study of RO4929097 with bevacizumab in patients with recurrent malignant glioma. J Neurooncol. 2016; 130(3): 571-579.
Wu Y, Chen M, Wu P, Chen C, Xu ZP, Gu W. Increased PD-L1 expression in breast and colon cancer stem cells. Clin Exp Pharmacol Physiol. 2017; 44(5): 602-604.
Deng Z, Wu Y, Ma W, Zhang S, Zhang YQ. Adoptive T-cell therapy of prostate cancer targeting the cancer stem cell antigen EpCAM. BMC Immunol. 2015; 16: 1.
Jachetti E, Caputo S, Mazzoleni S, Brambillasca CS, Parigi SM, Grioni M et al. Tenascin-C Protects Cancer Stem–like Cells from Immune Surveillance by Arresting T-cell Activation. Cancer Res. 2015; 75(10): 2095-108.
How to Cite
LicenseThe periodical offers access to content in the Open Access system under the Creative Commons non-exclusive license (CC BY-ND 4.0).
Number of views and downloads: 5
Number of citations: 0