The crossroads between cancer stem cells and aging

The cancer stem cell (CSC) hypothesis suggests that only a subpopulation of cells within a tumour is responsible for the initiation and progression of neoplasia. The original and best evidence for the existence of CSCs came from advances in the field of haematological malignancies. Thus far, putativ...

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Bibliographic Details
Published in:BMC cancer 2015-01, Vol.15 Suppl 1 (S1), p.S1-S1, Article S1
Main Authors: Santos Franco, Sara, Raveh-Amit, Hadas, Kobolák, Julianna, Alqahtani, Mohammed H, Mobasheri, Ali, Dinnyes, András
Format: Article
Language:English
Subjects:
Aging - physiology
Animals
Carcinogenesis
Epigenesis, Genetic
Humans
Neoplasms - genetics
Neoplasms - pathology
Neoplastic Stem Cells - physiology
Review
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Summary:The cancer stem cell (CSC) hypothesis suggests that only a subpopulation of cells within a tumour is responsible for the initiation and progression of neoplasia. The original and best evidence for the existence of CSCs came from advances in the field of haematological malignancies. Thus far, putative CSCs have been isolated from various solid and non-solid tumours and shown to possess self-renewal, differentiation, and cancer regeneration properties. Although research in the field is progressing extremely fast, proof of concept for the CSC hypothesis is still lacking and key questions remain unanswered, e.g. the cell of origin for these cells. Nevertheless, it is undisputed that neoplastic transformation is associated with genetic and epigenetic alterations of normal cells, and a better understanding of these complex processes is of utmost importance for developing new anti-cancer therapies. In the present review, we discuss the CSC hypothesis with special emphasis on age-associated alterations that govern carcinogenesis, at least in some types of tumours. We present evidence from the scientific literature for age-related genetic and epigenetic alterations leading to cancer and discuss the main challenges in the field.
ISSN:1471-2407
1471-2407
DOI:10.1186/1471-2407-15-S1-S1