Abstract
MYC is overexpressed by many human tumour types and has been shown to regulate cell functions that are required for tumorigenesis. It is not clear, however, which of its target genes mediate these effects. A series of recent studies have indicated that this could be a result of the fact that MYC binds and regulates up to 15% of all genes. Does MYC function as a widespread regulator of transcription or as a classical transcription factor that regulates a limited number of downstream targets?
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Acknowledgements
The following individuals provided helpful comments during the preparation of this review: M. Cole, C. Dang, S. Sykes and A. Norvell. This work was supported by grants to S.B.M. from the National Institutes of Health. In addition, this work was partially supported by funds from the Commonwealth Universal Research Enhancement Program, Pennsylvania Department of Health. Finally, we would like to add that many other groups have contributed data that were crucial to our current discussion of MYC function. Due to space limitations, these important contributions could not be highlighted in this review.
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Patel, J., Loboda, A., Showe, M. et al. Analysis of genomic targets reveals complex functions of MYC. Nat Rev Cancer 4, 562–568 (2004). https://doi.org/10.1038/nrc1393
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DOI: https://doi.org/10.1038/nrc1393
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