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 Blood, 15 January 2007, Vol. 109, No. 2, pp. 792-794.
Prepublished online as a Blood First Edition Paper on September 12, 2006; DOI 10.1182/blood-2006-07-033985.

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NEOPLASIA

Brief report

Regulation of the Arf tumor suppressor in Eµ-Myc transgenic mice: longitudinal study of Myc-induced lymphomagenesis

David Bertwistle1, and Charles J. Sherr2,

1 Department of Genetics & Tumor Cell Biology, Howard Hughes Medical Institute, Memphis, TN; 2 Department of Genetics & Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN

Lymphomagenesis in Eµ-Myc mice is opposed by the Arf tumor suppressor, whose inactivation compromises p53 function and accelerates disease. Finding nascent Eµ-Myc–induced tumors in which p19Arf causes cell-cycle arrest or apoptosis is problematic, since such cells will be eliminated until Arf or p53 function is lost. Knock-in mice expressing a green fluorescent protein (GFP) in lieu of Arf coding sequences allow analysis of Arfpromoter regulation uncoupled from p19Arf action. Prior to frank lymphoma development, unexpectedly low levels of Eµ-Myc–induced p19Arf or GFP were expressed. However, as lymphomas arose in Arf+/GFP heterozygotes, additional oncogenic events synergized with Eµ-Myc to further induce the functionally null Arf-Gfp allele. Concomitant up-regulation of p19Arf was not observed; instead, the wild-type allele was inactivated. We infer that very low levels of Arf are tumor suppressive, and that further induction provides the selective pressure for the emergence of tumors that have inactivated the gene.


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