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Abstract
The basic helix-loop-helix protein Myc is a renowned transcription factor controlling
disparate aspects of cell physiology that, together, allow efficient proliferation
of somatic cells. This ability, together with the observation that its deregulated
expression occurs in the majority of human cancers, suggests that Myc could be a good
therapeutic target. However, several aspects of Myc biology remain elusive: what is
the major difference between oncogenic and physiological Myc? How does oncogenic Myc
evade the intrinsic tumor surveillance pathways provided by evolution? If Myc inhibition
were even possible, what would be the consequences for the homeostasis of normal proliferating
tissues versus the fate of cancer cells? Here we summarize the latest works addressing
these issues.
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