Research ArticleCancer

Targeting of AML1-ETO in t(8;21) Leukemia by Oridonin Generates a Tumor Suppressor–Like Protein

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Science Translational Medicine  28 Mar 2012:
Vol. 4, Issue 127, pp. 127ra38
DOI: 10.1126/scitranslmed.3003562

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Herbal Fusion

High-tech gadgets and designer medicines increasingly drive medical treatment. But newer isn’t always better, and there has been a revitalized push for “natural” and “herbal” remedies. Although evidence supporting some of these therapies is shaky at best, researchers have found solid scientific bases for others—isolating active compounds with well-established biological function. One such compound is oridonin. Originally identified as a component of the herb Isodon rubescens, oridonin selectively kills leukemic cells that express a particular oncoprotein. Now, Zhen et al. show us exactly how compound works.

Acute myeloid leukemia (AML) is a cancer of myeloid cells in the blood and bone marrow. The AML1-ETO fusion protein—an oncoprotein that results from a chromosomal translocation found in a subset of AML patients—is cleaved as a result of oridonin exposure. In the current study, the authors demonstrated that oridonin has two functions within AML1-ETO+ AML cells. The drug bound and blocked components of the oxidative damage prevention system, glutathione and thioredoxin/thioredoxin reductase, which resulted in increased amounts of reactive oxygen species and activated caspase-3. Oridonin also specifically bound to AML1-ETO, causing it to be cleaved into a truncated version that acted as a tumor suppressor in the AML cells. These data show how a simple herb can contribute a lead compound for personalized therapy in AML1-ETO+ AML patients.

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