The epigenetic/noncoding origin of tumor dormancy

Crea, Francesco; Nur Saidy, Nur Ridzwan; Collins, Colin C. and Wang, Yuzhuo (2015). The epigenetic/noncoding origin of tumor dormancy. Trends in molecular medicine, 21(4) pp. 206–11.

DOI: https://doi.org/10.1016/j.molmed.2015.02.005

Abstract

Cancer stem cells (CSCs) have been implicated as the seeds of treatment resistance and metastasis, which are the most deadly features of a neoplasm. However, an unequivocal definition of the CSC phenotype is still missing. A common feature of normal and aberrant stem cells is their ability to enter a prolonged dormant state. Cancer dormancy is a key mechanism for treatment resistance and metastasis. Here we propose a unified definition of dormancy-competent CSCs (DCCs) as the neoplastic subpopulation that can plastically alternate periods of dormancy and rapid growth. Irreversible DNA mutations can hardly account for this versatile behavior, and based on emerging evidence we propose that cancer dormancy is a nongenetic disease driven by the flexible nature of the epigenetic/noncoding interactome.

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About

• Item ORO ID
• 45783
• Item Type
• Journal Item
• ISSN
• 1471-499X
• Project Funding Details

• Funded Project Name	Project ID	Funding Body
  Not Set	5629	Michael Smith Foundation for Health Research
  Not Set	Not Set	Prostate Cancer Foundation BC

• Keywords
• dormancy; dormancy-competent cancer stem cells; epigenetic/noncoding interactome; metastasis; therapy resistance
• Academic Unit or School
• Faculty of Science, Technology, Engineering and Mathematics (STEM) > Life, Health and Chemical Sciences
  Faculty of Science, Technology, Engineering and Mathematics (STEM)
• Research Group
• Cancer Research Group
• Copyright Holders
• © 2016 Elsevier
• Depositing User
• Francesco Crea