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

• DOI: 10.1126/scitranslmed.3003562
• Publication Date: 2012-03-28T19:24:32Z
• Authors: Tao Zhen; Chuan-Feng Wu; Ping Liu; Hai-Yan Wu; Guang-Biao Zhou; Ying Lu; Jian-Xiang Liu; Yang Liang; Keqin Kathy Li; Yue-Ying Wang; Yin-Yin Xie; Miao-Miao He; Huang-Ming Cao; Wei-Na Zhang; Li-Min Chen; Kevin Petrie; Sai-Juan Chen; Zhu Chen
• Keywords: 0301 basic medicine; Oncogene Proteins, Fusion; Chromosomes, Human, Pair 21; Intracellular Space; Models, Biological; Translocation, Genetic; Mice; 03 medical and health sciences; RUNX1 Translocation Partner 1 Protein; Animals; Humans; Molecular Targeted Therapy; sub_healthsciences; Caspase 3; Protein Stability; 3. Good health; Enzyme Activation; Mice, Inbred C57BL; Leukemia, Myeloid, Acute; Core Binding Factor Alpha 2 Subunit; Neoplastic Stem Cells; Diterpenes, Kaurane; Reactive Oxygen Species; sub_biomedicalsciences; Chromosomes, Human, Pair 8

Oridonin treats AML by generating a truncated version of the AML1-ETO oncoprotein that functions as a tumor suppressor.