Implications of the cancer stem-cell hypothesis for breast cancer prevention and therapy

J Clin Oncol. 2008 Jun 10;26(17):2813-20. doi: 10.1200/JCO.2008.16.3931.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • BRCA1 Protein / metabolism
  • Biomarkers, Tumor / metabolism
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Breast Neoplasms / prevention & control
  • Breast Neoplasms / therapy*
  • Cell Differentiation
  • Cell Proliferation
  • Cell Transformation, Neoplastic / pathology
  • Drug Resistance, Neoplasm*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Hedgehog Proteins / metabolism
  • Humans
  • Neoplasm Metastasis
  • Neoplastic Stem Cells / drug effects*
  • Neoplastic Stem Cells / metabolism
  • Neoplastic Stem Cells / pathology
  • Neoplastic Stem Cells / radiation effects*
  • PTEN Phosphohydrolase / metabolism
  • Radiotherapy
  • Receptor, ErbB-2 / metabolism
  • Receptors, Notch / metabolism
  • Signal Transduction
  • Treatment Failure
  • Wnt Proteins / metabolism

Substances

  • Antineoplastic Agents
  • BRCA1 Protein
  • Biomarkers, Tumor
  • Hedgehog Proteins
  • Receptors, Notch
  • Wnt Proteins
  • Receptor, ErbB-2
  • PTEN Phosphohydrolase