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Nat Rev Cancer. 2014 Sep;14(9):611-22. doi: 10.1038/nrc3793. Epub 2014 Aug 14.

Mechanisms of disseminated cancer cell dormancy: an awakening field.

Author information

1
1] Division of Hematology and Oncology, Department of Medicine, Department of Otolaryngology, Tisch Cancer Institute, New York NY 10029, USA. [2] Black Family Stem Cell Institute, Ichan School of Medicine at Mount Sinai, New York NY 10029, USA. [3].
2
1] Division of Hematology and Oncology, Department of Medicine, Department of Otolaryngology, Tisch Cancer Institute, New York NY 10029, USA. [2] Black Family Stem Cell Institute, Ichan School of Medicine at Mount Sinai, New York NY 10029, USA. [3] Molecular and Translational Oncology Laboratory, Institut d'Investigacions Biomèdiques August Pi I Sunyer, Barcelona 08036, Spain. [4].
3
1] Division of Hematology and Oncology, Department of Medicine, Department of Otolaryngology, Tisch Cancer Institute, New York NY 10029, USA. [2] Black Family Stem Cell Institute, Ichan School of Medicine at Mount Sinai, New York NY 10029, USA.

Abstract

Metastases arise from residual disseminated tumour cells (DTCs). This can happen years after primary tumour treatment because residual tumour cells can enter dormancy and evade therapies. As the biology of minimal residual disease seems to diverge from that of proliferative lesions, understanding the underpinnings of this new cancer biology is key to prevent metastasis. Analysis of approximately 7 years of literature reveals a growing focus on tumour and normal stem cell quiescence, extracellular and stromal microenvironments, autophagy and epigenetics as mechanisms that dictate tumour cell dormancy. In this Review, we attempt to integrate this information and highlight both the weaknesses and the strengths in the field to provide a framework to understand and target this crucial step in cancer progression.

PMID:
25118602
PMCID:
PMC4230700
DOI:
10.1038/nrc3793
[Indexed for MEDLINE]
Free PMC Article

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