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Stem Cells and Colon Cancer

Stem Cells

  1. Simone Di Franco1,
  2. Antonina Benfante1,
  3. Flora Iovino1,
  4. Sebastiano Bonventre1,
  5. Francesco Dieli2,
  6. Giorgio Stassi1,3,
  7. Matilde Todaro1

Published Online: 15 JUL 2012

DOI: 10.1002/3527600906.mcb.201100021

Reviews in Cell Biology and Molecular Medicine

Reviews in Cell Biology and Molecular Medicine

How to Cite

Di Franco, S., Benfante, A., Iovino, F., Bonventre, S., Dieli, F., Stassi, G. and Todaro, M. 2012. Stem Cells and Colon Cancer. Reviews in Cell Biology and Molecular Medicine. .

Author Information

  1. 1

    University of Palermo, Department of Surgical and Oncological Sciences, Cellular and Molecular Pathophysiology Laboratory, Palermo (PA), Italy

  2. 2

    University of Palermo, Division of Immunology and Immunogenetics, Department of Biotechnology and Medical and Forensic Biopathological (DIBIMEF), Palermo (PA), Italy

  3. 3

    IRCCS Fondazione Salvatore Maugeri, Department of Cellular and Molecular Oncology, Pavia (PV), Italy

Publication History

  1. Published Online: 15 JUL 2012


The current concept of tumorigenesis suggests that cancers arise and are “driven” by cells with stem cell-like properties, known as cancer stem cells (CSCs), which share many functional and molecular features with normal stem cells. Self-renewal key pathways (e.g., Wnt, Notch, and Hedgehog) are tightly regulated in normal stem cells, but are impaired in CSCs. For instance, active Wnt pathway plays a crucial role in colon cancer pathophysiology, where deregulation of the adenomatous polyposis coli (APC) gene, a negative regulator of Wnt signaling, represents one of the earliest alterations in the multistep process of colon carcinogenesis, causing early adenoma formation. Normal colon stem cells reside at the base of the crypts, in specialized regions termed “niches,” that provide a microenvironment structured to ensure their self-renewal. It is becoming increasingly clear that CSCs are involved in tumor recurrence and resistance to conventional therapies, due to high expression levels of ATP-binding cassette (ABC) transporters, slow cycling rates, and the presence of cytoprotective factors. Future therapeutic strategies should selectively target CSCs for a complete clinical remission.


  • Stem cell;
  • Colon cancer stem cell;
  • Crypt;
  • Niche