Yali Dou, PhD
Associate Professor, University of Michigan
Education
1991-1996 BS, Basic Medicine, Beijing Medical University (now Peking University Health Center)
1996-1998 MS, Molecular Biology, University of Rochester
1996-2000 PhD, Mentor: Martin A. Gorovsky, University of Rochester
Dissertation: The function of linker histone phosphorylation in
Tetrahymena Thermophila
Postdoctoral training
10/2000-9/2002 Postdoctoral Fellow (with Dr. Martin A. Gorovsky), University of Rochester
10/2002-9/2006 Postdoctoral Fellow (with Dr. Robert G. Roeder), The Rockefeller University
ACAdemic appointments
9/2012- Associate Professor, Department of Pathology and Biological Chemistry, University of
Michigan
10/2006-8/2012 Assistant Professor, Department of Pathology, University of Michigan
12/2006-8/2012 Assistant Professor, Department of Biological Chemistry, University of
Michigan
Topic: Targeting MLL in acute myeloid leukemia
Abstract:
Abnormal transmission of epigenetic information contributes to human pathology, such as the sequential progression of cancer. One of such epigenetic regulators is Mixed Lineage Leukemia (MLL) protein, which was originally cloned by its direct involvement in a group of distinct human acute leukemia with extremely poor prognosis. MLL gene abnormalities account for 5% to 10% of the disease, and at least 70% of the cases in infants under 1 year old. It is general consensus that MLL mutations disrupt expression of specific genes that are important in early blood cell development. MLL is a histone methyltransferase that modify histone H3 at lysine 4. This activity is essential for pathogenesis of mixed lineage leukemia and is tightly regulated by several highly conserved proteins. By using the mechanism based rational design, we have developed a novel inhibitor that targets the MLL methyltransferase activity. It shows profound efficacy against human and murine MLL-fusion leukemia cell lines by promoting apoptosis and differentiation of leukemia stem cells. Its mode of action is due to inhibition of expression of MLL target genes by reducing H3 K4 methylation. Our studies establish a proof-of-concept that targeting MLL is a valid strategy and provide a promising new agent for treatment of acute leukemia.
Venue: Room143, New Biology Building, THU
Time: Dec 25 (Tuesday), 2012; 16:30
Host: Prof. Haitao Li
