Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2013 Aug 27:4:225.
doi: 10.3389/fphys.2013.00225. eCollection 2013.

Breast cancer stem cells

Affiliations

Breast cancer stem cells

Thomas W Owens et al. Front Physiol. .

Abstract

Cancer metastasis, resistance to therapies and disease recurrence are significant hurdles to successful treatment of breast cancer. Identifying mechanisms by which cancer spreads, survives treatment regimes and regenerates more aggressive tumors are critical to improving patient survival. Substantial evidence gathered over the last 10 years suggests that breast cancer progression and recurrence is supported by cancer stem cells (CSCs). Understanding how CSCs form and how they contribute to the pathology of breast cancer will greatly aid the pursuit of novel therapies targeted at eliminating these cells. This review will summarize what is currently known about the origins of breast CSCs, their role in disease progression and ways in which they may be targeted therapeutically.

Keywords: breast cancer; cancer stems cells; cell fate; mammary gland; transcription factors.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Models of CSC formation. In the linear hierarchy model of CSC formation, the transformation events that drive tumorigenesis occur in a stem or progenitor cell that then gives rise to more differentiated progeny as the tumor develops. These differentiated progeny have reduced tumor-forming potential. In the second model, cancer stem cells evolve, perhaps via induction of EMT, either as part of disease progression or in response to selective pressures in the tumor microenvironment.

References

    1. Abraham B. K., Fritz P., McClellan M., Hauptvogel P., Athelogou M., Brauch H. (2005). Prevalence of CD44+/CD24-/low cells in breast cancer may not be associated with clinical outcome but may favor distant metastasis. Clin. Cancer Res. 11, 1154–1159 10.1158/1078-0432.CCR-06-0169 - DOI - PubMed
    1. Al-Hajj M., Wicha M. S., Benito-Hernandez A., Morrison S. J., Clarke M. F. (2003). Prospective identification of tumorigenic breast cancer cells. Proc. Natl. Acad. Sci. U.S.A. 100, 3983–3988 10.1073/pnas.0530291100 - DOI - PMC - PubMed
    1. Balic M., Lin H., Young L., Hawes D., Giuliano A., McNamara G., et al. (2006). Most early disseminated cancer cells detected in bone marrow of breast cancer patients have a putative breast cancer stem cell phenotype. Clin. Cancer Res. 12, 5615–5621 10.1158/1078-0432.CCR-06-0169 - DOI - PubMed
    1. Beltran A. S., Rivenbark A. G., Richardson B. T., Yuan X., Quian H., Hunt J. P., et al. (2011). Generation of tumor-initiating cells by exogenous delivery of OCT4 transcription factor. Breast Cancer Res. 13, R94 10.1186/bcr3019 - DOI - PMC - PubMed
    1. Chaffer C. L., Brueckmann I., Scheel C., Kaestli A. J., Wiggins P. A., Rodrigues L. O., et al. (2011). Normal and neoplastic nonstem cells can spontaneously convert to a stem-like state. Proc. Natl. Acad. Sci. U.S.A. 108, 7950–7955 10.1073/pnas.1102454108 - DOI - PMC - PubMed

LinkOut - more resources