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Implications of the Cancer Stem-Cell Hypothesis for Breast Cancer Prevention and Therapy

Madhuri Kakarala, Max S. Wicha

From the University of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI

Corresponding author: Max S. Wicha, MD, University of Michigan Comprehensive Cancer Center, 1500 East Medical Center Dr, 6302 CC, Ann Arbor, MI 48109-5942; e-mail: mwicha{at}umich.edu

Recent research in breast biology has provided support for the cancer stem-cell hypothesis. Two important components of this hypothesis are that tumors originate in mammary stem or progenitor cells as a result of dysregulation of the normally tightly regulated process of self-renewal. As a result, tumors contain and are driven by a cellular subcomponent that retains key stem-cell properties including self-renewal, which drives tumorigenesis and differentiation that contributes to cellular heterogeneity. Advances in stem-cell technology have led to the identification of stem cells in normal and malignant breast tissue. The study of these stem cells has helped to elucidate the origin of the molecular complexity of human breast cancer. The cancer stem-cell hypothesis has important implications for early detection, prevention, and treatment of breast cancer. Both hereditary and sporadic breast cancers may develop through dysregulation of stem-cell self-renewal pathways. These aberrant stem cells may provide targets for the development of cancer prevention strategies. Furthermore, because breast cancer stem cells may be highly resistant to radiation and chemotherapy, the development of more effective therapies for this disease may require the effective targeting of this cell population.

Supported by National Institutes of Health Grants No. CA101860, CA66233, and P 30 C CA46592, and by the Taubman Institute.

Authors’ disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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