Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Front Endocrinol (Lausanne). 2012 Oct 23;3:125. doi: 10.3389/fendo.2012.00125. eCollection 2012.

Cancer stem cells, tumor dormancy, and metastasis.

Author information

  • 1Department of Pharmacological Sciences, Stony Brook University Stony Brook, NY, USA.

Abstract

Tumor cells can persist undetectably for an extended period of time in primary tumors and in disseminated cancer cells. Very little is known about why and how these tumors persist for extended periods of time and then evolve to malignancy. The discovery of cancer stem cells (CSCs) in human tumors challenges our current understanding of tumor recurrence, drug resistance, and metastasis, and opens up new research directions on how cancer cells are capable of switching from dormancy to malignancy. Although overlapping molecules and pathways have been reported to regulate the stem-like phenotype of CSCs and metastasis, accumulated evidence has suggested additional clonal diversity within the stem-like cancer cell subpopulation. This review will describe the current hypothesis linking CSCs and metastasis and summarize mechanisms important for metastatic CSCs to re-initiate tumors in the secondary sites. A better understanding of CSCs' contribution to clinical tumor dormancy and metastasis will provide new therapeutic revenues to eradicate metastatic tumors and significantly reduce the mortality of cancer patients.

KEYWORDS:

EMT–MET cooperativity; cancer stem cells; disseminated CSCs; metastasis; stem-like subpopulations; tumor dormancy

PMID:
23109929
[PubMed]
PMCID:
PMC3478572
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Frontiers Media SA Icon for PubMed Central
    Loading ...
    Write to the Help Desk