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Curr Cancer Drug Targets. 2003 Jun;3(3):163-75.

The MYC oncogene as a cancer drug target.

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Molecular Oncology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18A, D-82152 Martinsried, Germany.


The universal deregulation of c-myc gene expression in tumor cells suggests that this oncogene represents an attractive target for cancer therapeutic purposes. The same applies to the N-myc gene, which has a more restricted tissue specificity. Translocation (e.g., c-myc in Burkitt's lymphoma), or amplification (e.g., N-myc in neuroblastoma) of myc genes has been causally linked to tumor formation. Furthermore, the c-myc promoter integrates diverse mitogenic signalling cascades, which are constitutively activated in tumor cells, and translates them into expression of the c-MYC transcription factor, which promotes cell proliferation by regulating the expression of numerous target genes. Recent experimental data suggest, that even a brief inhibition of c-myc expression may be sufficient to permanently stop tumor growth and induce regression of tumors. Attempts to identify specific inhibitors of c-MYC/MAX dimerization have yielded promising results. In addition, downstream-target genes of c-MYC represent attractive targets for tumor therapy. Tumor cells expressing c-MYC at elevated levels are sensitized to treatment with DNA-damaging drugs. In mice and presumably also in human patients, the successful treatment of c-myc-induced tumors with conventional chemotherapy depends on the presence of functional p53. Therefore, restoration of this pathway, which is commonly lost in cancer cells, may enhance therapy of c-myc-induced tumors. These and other recent developments, which address the use of myc genes as therapeutic targets for cancer treatment, are discussed in this review.

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