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. Author manuscript; available in PMC: 2013 Mar 30.
Published in final edited form as: Cell. 2012 Mar 30;149(1):22–35. doi: 10.1016/j.cell.2012.03.003

Figure 1.

Figure 1

Figure 1

A. The MYC protooncogene is depicted downstream of receptor signal transduction pathways, which elicit positive or negative regulation of the MYC gene. MYC produces the transcription factor Myc, which dimerizes with Max and bind target DNA sequences or E-boxes (with the sequence 5′-CANNTG-3′) to regulate transcription of genes involved in cell growth and proliferation. The WNT pathway is depicted with APC negatively regulating β-catenin, which upon nuclear translocation participates in the transactivation of MYC, such that loss of APC results in constitutive oncogenic MYC expression. B. When MYC is deregulated, by gene amplication, chromosomal translocation or loss of upstream regulators, such as APC, acute sustained oncogenic MYC expression results in checkpoint activation p53 or Arf. Loss of checkpoint regulation through mutations of p53 or Arf, for example, uncloaks MYC’s full tumorigenic potential.