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Interaction of Cell-Cycle Checkpoints with Muscle Differentiation

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Part of the book series: Contemporary Cancer Research ((CCR))

Abstract

Damage to genomic DNA occurs spontaneously in all living cells, and represents a significant and constant problem. In addition, chemical or physical mutagens can cause a variety of DNA lesions, including base modifications, intra- and interstrand crosslinks and single- or double-strand breaks (31). If left unrepaired, these DNA lesions can lead to mutations or loss of viability. Thus, cell-cycle checkpoints and DNA-repair mechanisms have evolved to ensure cellular survival in the face of DNA damage. Multicellular organisms have additional issues to deal with, including differentiation programs, as well as the existence of a limited number of stem cells required for renewal and repair of differentiated tissues. Because cell-cycle checkpoints and differentiation utilize the same key cell-cycle regulatory factors to mediate cell-cycle arrest, multicellular organism must integrate these two processes simultaneously. The subject of this chapter is the intersection of genetic alterations in the DNA damage-response pathway that interfere with overt differentiation.

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Fiddler, T., Huang, J., Ostermeyer, E., Johnson-Pais, T., Thayer, M.J. (2001). Interaction of Cell-Cycle Checkpoints with Muscle Differentiation. In: Nickoloff, J.A., Hoekstra, M.F. (eds) DNA Damage and Repair. Contemporary Cancer Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-095-7_12

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