Journal of Alzheimers Disease & Parkinsonism
Open Access

Review Article

Neural Cancer Stem Cells: Focusing on Chromosome Ends

Fernando Pires Hartwig^*

Postgraduate Program in Epidemiology, Federal University of Pelotas, Oncology Research Group, Technology Development Center (Biotechnology Unit), Federal University of Pelotas, Brazil

Corresponding Author:

Fernando Pires Hartwig
Postgraduate Program in Epidemiology
Federal University of Pelotas, Oncology Research Group
Technology Development Center (Biotechnology Unit)
Federal University of Pelotas, Brazil
Tel: (5553)81347172
E-mail: fernandophartwig@gmail.com

Received date: June 10, 2013; Accepted date: June 24, 2013; Published date: June 26, 2013

Citation: Hartwig FP (2013) Neural Cancer Stem Cells: Focusing on Chromosome Ends. J Alzheimers Dis Parkinsonism 3:115. doi: 10.4172/2161-0460.1000115

Copyright: © 2013 Hartwig FP. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Telomeres are DNA tandem repeats associated with six proteins located at chromosome ends. Telomere shortening happens after each replication round in the majority of human cells, including adult stem cells, leading to telomere dysfunction and activation of senescence and/or apoptosis. In this commentary, key studies evidencing that telomerase overexpression (which is the most common telomere lengthening mechanism in cancer) confer stem-like properties to neural cells with tumorigenic potential, which is in accordance to previously proposed models of TERT overexpression as a mechanism for the emergence of neural cancer stem cells. In addition, the recent finding that telomerase inhibition is a promising anti-neural cancer stem cell therapy (at least in gliomas) is confronted with other studies, resulting in the identification of potential limitations: the presence of alternative lengthening of telomeres in neural cancer stem cells (already identified in glioma stem cells) and of the possibility that short telomeres is not an universal feature of neural cancer stem cells. Further investigation regarding telomere length measurement in neural cancer stem cells of different origins and development of clinically feasible and applicable methods to distinguish telomerase-positive from ALT-positive neural cancer stem cells are pointed as important perspectives to better understand the potential of the promising telomerase inhibition-based therapy to fight neural cancer stem cells.

Keywords