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. 2005 May;7(5):433-44.
doi: 10.1016/j.ccr.2005.03.036.

Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation

Jonas A Nilsson  1 , Ulrich B Keller, Troy A Baudino, Chunying Yang, Sara Norton, Jennifer A Old, Lisa M Nilsson, Geoffrey Neale, Debora L Kramer, Carl W Porter, John L Cleveland
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Free article

Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation

Jonas A Nilsson et al. Cancer Cell. 2005 May.
Free article

Abstract

Checkpoints that control Myc-mediated proliferation and apoptosis are bypassed during tumorigenesis. Genes encoding polyamine biosynthetic enzymes are overexpressed in B cells from E mu-Myc transgenic mice. Here, we report that disabling one of these Myc targets, Ornithine decarboxylase (Odc), abolishes Myc-induced suppression of the Cdk inhibitors p21(Cip1) and p27(Kip1), thereby impairing Myc's proliferative, but not apoptotic, response. Moreover, lymphoma development was markedly delayed in E mu-Myc;Odc(+/-) transgenic mice and in E mu-Myc mice treated with the Odc inhibitor difluoromethylornithine (DFMO). Strikingly, tumors ultimately arising in E mu-Myc;Odc(+/-) transgenics lacked deletions of Arf, suggesting that targeting Odc forces other routes of transformation. Therefore, Odc is a critical Myc transcription target that regulates checkpoints that guard against tumorigenesis and is an effective target for cancer chemoprevention.

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