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• W2004098260 abstract "Abstract Neuroblastoma is a pediatric malignancy that arises from the neural crest, and patients with high-risk neuroblastoma, which typically harbor amplifications of MYCN, have an extremely poor prognosis. The tyrosine hydroxylase (TH) promoter-driven TH-MYCN transgenic mouse model faithfully recapitulates many hallmarks of human MYCN-amplified neuroblastoma. A key downstream target of Myc oncoproteins in tumorigenesis is ornithine decarboxylase (Odc), the rate-limiting enzyme of polyamine biosynthesis. Indeed, sustained treatment with the Odc suicide inhibitor α-difluoromethylornithine (DFMO) or Odc heterozygosity markedly impairs lymphoma development in Eμ-Myc transgenic mice, and these effects are linked to the induction of the cyclin-dependent kinase (Cdk) inhibitor p27Kip1, which is normally repressed by Myc. Here, we report that DFMO treatment, but not Odc heterozygosity, impairs MYCN-induced neuroblastoma and that, in this malignancy, transient DFMO treatment is sufficient to confer protection. The selective anticancer effects of DFMO on mouse and human MYCN-amplified neuroblastoma also rely on its ability to disable the proliferative response of Myc, yet in this tumor context, DFMO targets the expression of the p21Cip1 Cdk inhibitor, which is also suppressed by Myc oncoproteins. These findings suggest that agents, such as DFMO, that target the polyamine pathway may show efficacy in high-risk, MYCN-amplified neuroblastoma. [Cancer Res 2009;15(4):547–53]" @default.
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• W2004098260 date "2009-01-15" @default.
• W2004098260 modified "2023-10-12" @default.
• W2004098260 title "Targeting Ornithine Decarboxylase Impairs Development of <i>MYCN</i>-Amplified Neuroblastoma" @default.
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• W2004098260 doi "https://doi.org/10.1158/0008-5472.can-08-2968" @default.
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