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