Abstract
The classical cancer stem cell (CSC) model places CSCs at the apex of a hierarchical scale, suggesting different genetic alterations in non-CSCs compared to CSCs, since an ill-defined number of cell generations and time intervals separate CSCs from the more differentiated cancer cells that form the bulk of the tumor. Another model, however, poses that CSCs should be considered a functional state of tumor cells, hence sharing the same genetic alterations. Here, we review the existing literature on the genetic landscape of CSCs in various tumor types and as a case study investigate the genomic complexity of DNA obtained from matched CSCs and non-CSCs from five ovarian cancer patients, using a genome-wide single-nucleotide polymorphism (SNP) microarray.
Highlights
IntermIendcioantetr, ahsitgtho)thaerehireerparrechseicnatlemd.odel, an alternative theory poses cancer stem cell (CSCs) as a functional state of a tumor cell
The classical CSC model places CSCs at the apex of a hierarchical scale, implying different genetic alterations in non-CSCs compared to CSCs, since a number of cell generations and time intervals separate CSCs from the more differentiated cancer cells that form the bulk of the tumor (Figure 1)
CSCs seem to be endowed with more efficient DNA repair mechanisms, which partially shield their genome from genotoxic events
Summary
CSCs have been identified in most tumor types (both solid and liquid) based on the expression of specific surface markers, lack of certain differentiation markers and high tumorigenic potential. Most studies analyzed either tumor cell lines or a small number of primary samples, due to the difficulty of obtaining enough genomic DNA from CSCs. CSC isolation was often not performed according to stemness marker expression, but rather by using in vitro specific cell culture protocols. When cultured in serum-supplemented media, glioblastoma cells underwent genomic rearrangements in terms of loss of heterozygosity (LOH), pseudo-tetraploidy and chromosomal deletions, suggesting a key role of in vitro culture conditions in the acquisition of genetic instability. It is unknown whether these in vitro findings can be relevant to CSCs from patients. Conclusions suggest that CSCs and bulk tumor cells share the same genetic alterations but GBM presents substantial intra-tumor genetic heterogeneity [11]
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