Lessons from development: A role for asymmetric stem cell division in cancer |
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Authors: | Anne E Powell Chia-Yi Shung Katherine W Saylor Karin A Müllendorf Joseph B Weiss Melissa H Wong |
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Institution: | 1. Department of Cell and Developmental Biology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA;2. Shriners Hospital for Children Research Division, Portland, OR 97239, USA;3. The Vollum Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA;4. Department of Cardiology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA;5. Department of Dermatology, Oregon Stem Cell Center, Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA |
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Abstract: | Asymmetric stem cell division has emerged as a major regulatory mechanism for physiologic control of stem cell numbers. Reinvigoration of the cancer stem cell theory suggests that tumorigenesis may be regulated by maintaining the balance between asymmetric and symmetric cell division. Therefore, mutations affecting this balance could result in aberrant expansion of stem cells. Although a number of molecules have been implicated in regulation of asymmetric stem cell division, here, we highlight known tumor suppressors with established roles in this process. While a subset of these tumor suppressors were originally defined in developmental contexts, recent investigations reveal they are also lost or mutated in human cancers. Mutations in tumor suppressors involved in asymmetric stem cell division provide mechanisms by which cancer stem cells can hyperproliferate and offer an intriguing new focus for understanding cancer biology. Our discussion of this emerging research area derives insight from a frontier area of basic science and links these discoveries to human tumorigenesis. This highlights an important new focus for understanding the mechanism underlying expansion of cancer stem cells in driving tumorigenesis. |
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