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5 - Preventative and therapeutic strategies for cancer stem cells

from SECTION II - THERAPEUTIC IMPLICATIONS OF CANCER STEM CELLS

Published online by Cambridge University Press:  15 December 2009

By
Stewart Sell  and
Gennadi Glinsky
Edited by
William L. Farrar
Stewart Sell
Affiliation:
Wadsworth Center, Ordway Research Institute, and the University at Albany
Gennadi Glinsky
Affiliation:
Ordway Research Institute
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Summary

Treatment of cancer should be directed to cancer stem cells as well as to the stage of maturation arrest at which the cancer cells accumulate. Cancers contain the same cell populations as do normal adult tissues: stem cells, proliferating transit-amplifying cells, terminally differentiated (mature cells), and dead cells. During normal tissue renewal, the number of proliferating transit-amplifying cells is essentially the same as the number of terminally differentiating cells so that the total number of cells remains relatively constant. On the other hand, in cancer tissue, the transit-amplifying cells are arrested at a stage of maturation in which they continue to proliferate and accumulate so that the mass of cancerous tissue continues to increase. The ability of retinoic acids to induce differentiation of teratocarcinoma stem cells provided a proof of principle that cancer stem cells could be induced to differentiate (differentiation therapy). Differentiation therapy has been applied with great success to cancer of the blood cells (leukemias) by inactivation of the signaling pathways that allow the leukemic transit-amplifying cells to continue to proliferate and not die (maturation arrest). Conventional therapies, such as chemotherapy, radiotherapy, and antiangiogenic therapies, also act on the proliferating cancer transit-amplifying cells. When these therapies are discontinued, the cancer will reform from the therapy-resistant cancer stem cells. Cancer stem cell–directed therapy may be possible using small inhibitory molecules or inhibitory RNAs (iRNA) to block the signals that maintain stemness so that the cancer stem cells are allowed to differentiate.

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Cancer Stem Cells , pp. 68 - 92
Publisher: Cambridge University Press
Print publication year: 2009

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