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Translocations involving c-myc and c-myc function

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Abstract

c-MYC is the prototype for oncogene activation by chromosomal translocation. In contrast to the tightly regulated expression of c-myc in normal cells, c-myc is frequently deregulated in human cancers. Herein, aspects of c-myc gene activation and the function of the c-Myc protein are reviewed. The c-myc gene produces an oncogenic transcription factor that affects diverse cellular processes involved in cell growth, cell proliferation, apoptosis and cellular metabolism. Complete removal of c-myc results in slowed cell growth and proliferation, suggesting that while c-myc is not required for cell proliferation, it acts as an integrator and accelerator of cellular metabolism and proliferation.

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Acknowledgements

Supported by National Institutes of Health Grant CA69322 (LM Boxer), CA51497 (CV Dang) and CA57431 (CV Dang). We thank E Emison, L Gardner, LA Lee and D Wechsler for comments.

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  1. Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, California, USA

    Linda M Boxer

  2. Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, Maryland, USA

    Chi V Dang

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Boxer, L., Dang, C. Translocations involving c-myc and c-myc function. Oncogene 20, 5595–5610 (2001). https://doi.org/10.1038/sj.onc.1204595

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