Article

Self-renewal and solid tumor stem cells.

University of Michigan Medical School, CCGC Room 4410, 1500 E Medical Center Drive, Ann Arbor 48109-0936, USA.
Oncogene (Impact Factor: 8.56). 10/2004; 23(43):7274-82. DOI: 10.1038/sj.onc.1207947
Source: PubMed

ABSTRACT Solid tumors arise in organs that contain stem cell populations. The tumors in these tissues consist of heterogeneous populations of cancer cells that differ markedly in their ability to proliferate and form new tumors. In both breast cancers and central nervous system tumors, cancer cells differ in their ability to form tumors. While the majority of the cancer cells have a limited ability to divide, a population of cancer stem cells that has the exclusive ability to extensively proliferate and form new tumors can be identified based on marker expression. Growing evidence suggests that pathways that regulate the self-renewal of normal stem cells are deregulated in cancer stem cells resulting in the continuous expansion of self-renewing cancer cells and tumor formation. This suggests that agents that target the defective self-renewal pathways in cancer cells might lead to improved outcomes in the treatment of these diseases.

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  • Source
    S Fagoonee, H Li, H Zhang, F Altruda, R Pellicano
    [Show abstract] [Hide abstract]
    ABSTRACT: The main function of gastric stem cells is to maintain the integrity of the gastrointestinal epithelium and replenish all the mature cell lineages. In order to accomplish this, gastric stem cells proliferate and self-renew, giving rise to transient amplifying cells which replace the constantly renewing epithelium, especially after injury induced by long-term inflammation. Gastric cancer (GC) remains the fourth most common cancer and the second leading cause of death for cancer in the world. The most accepted model of gastric carcinogenesis provides a multifactorial and multistep pathogenesis, involving a number of initiators and other continuator agents. Helicobacter pylori infection is recognized as a necessary but insufficient cause of GC. Recent advances in gastric stem cell biology point out to two hypotheses. In the first, it is postulated that resident stem cells may, in a chronically inflamed environment, as in the case of Helicobacter pylori-induced gastritis, accumulate over time a series of genetic and epigenetic changes that lead to the emergence of GC stem cells. Alternatively, the setting of chronic inflammatory stress may lead to loss of the indigenous gastric stem cells from their niches, followed by recruitment and engraftment of bone marrow derived stem cells (BMDCs) into the gastric epithelium. In the mouse model, increasing evidence supports the hypothesis that BMDCs are important cellular source of Helicobacter-induced GC. This review highlights data and hypotheses about GC as a model of stem-cell disease.
    Panminerva medica 12/2014; 56(4):289-300. · 2.28 Impact Factor

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