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
. 2011 Jun;7(2):128-135.
doi: 10.1007/s11888-011-0093-2.

Colorectal Cancer Stem Cells: Biology and Therapeutic Implications

Affiliations

Colorectal Cancer Stem Cells: Biology and Therapeutic Implications

Brian J Wilson et al. Curr Colorectal Cancer Rep. 2011 Jun.

Abstract

The hypothesis that cancer is driven by a subpopulation of tumor-initiating or cancer stem cells (CSC), defined by their selective ability for extensive self-renewal and capacity to give rise to nontumorigenic cancer cell progeny through differentiation, has been validated experimentally in diverse human malignancies. Translational relevance of the CSC hypothesis is underlined by emerging novel strategies designed to target all subpopulations within a given tumor in order to effect cancer eradication and improve patient outcomes. Colorectal cancer stem cells (CRSCs) have been identified and successfully isolated by several research groups based on distinct cell-surface marker characteristics. Identification of CRSC populations has led to a wave of discoveries describing novel self-renewal and drug resistance mechanisms in colorectal cancer that represent novel future therapeutic targets. In this review, we will discuss emerging CRSC-specific pathways and the therapeutic promise of targeting this cancer population in colorectal cancer patients.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Targeting colorectal cancer stem cells (CRSCs) versus conventional therapies. Top: Conventional therapies, including chemotherapies and radiotherapies, target the bulk population of rapidly proliferating colorectal cancer cells, resulting in removal of a large proportion of tumor mass. However, therapy-resistant CRSCs remain (cell indicated in yellow) and can differentiate into non-CRSC cancer cells and repopulate the tumor over time, resulting in a more aggressive phenotype than the initial pretreated malignancy. Bottom: Targeting of the CRSC subpopulation is hypothesized to remove the cells responsible for tumorigenesis resulting in tumor regression, ultimate remission, and cure of the colorectal cancer

References

    1. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2008. CA Cancer J Clin. 2008;58:71–96. - PubMed
    1. Markowitz SD, Bertagnolli MM. Molecular origins of cancer: molecular basis of colorectal cancer. N Engl J Med. 2009;361:2449–60. - PMC - PubMed
    1. Frank NY, Schatton T, Frank MH. The therapeutic promise of the cancer stem cell concept. J Clin Invest. 2010;120:41–50. - PMC - PubMed
    1. Zhou BB, Zhang H, Damelin M, et al. Tumour-initiating cells: challenges and opportunities for anticancer drug discovery. Nat Rev Drug Discov. 2009;8:806–23. - PubMed
    1. Vogelstein B, Fearon ER, Hamilton SR, et al. Genetic alterations during colorectal-tumor development. N Engl J Med. 1988;319:525–32. - PubMed

LinkOut - more resources