Conditional transgenic models define how MYC initiates and maintains tumorigenesis

Constadina Arvanitis, Dean W. Felsher*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

111 Scopus citations


MYC is one of the most commonly overexpressed oncogenes in human cancer. The targeted inactivation of MYC is a possible therapy for neoplasia. Conditional transgenic mouse model systems are tractable methods to precisely dissect how and when the inactivation of MYC might be effective in the treatment for human cancer. From these model systems, several general principles emerge. MYC inactivation stereotypically results in the proliferative arrest, differentiation and/or apoptosis of tumor cells. The specific consequences of MYC inactivation appear to depend both on the type of cancer as well as the constellation of genetic events unique to a given tumor. Tumors can escape from dependence upon MYC by acquiring compensatory genetic events. MYC inactivation can uncover the stem cell properties of tumor cells that differentiate into normal appearing cells. In some cases, these differentiated cells are actually dormant tumor cells that recover their neoplastic properties upon MYC reactivation. In other cases, even brief MYC inactivation is sufficient to induce sustained tumor regression. Insights from conditional transgenic mouse models will be useful in the development of therapies that target MYC for the treatment of cancer.

Original languageEnglish (US)
Pages (from-to)313-317
Number of pages5
JournalSeminars in Cancer Biology
Issue number4
StatePublished - Aug 1 2006


  • MYC
  • Transgenic models
  • Tumorigenesis

ASJC Scopus subject areas

  • Cancer Research

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