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32nd IRCMS Seminar

December 20 2017

We would like to inform you that the 32nd IRCMS Seminar has been scheduled as below. We would be pleased to see many of you participating in the seminar.

 

Date       :   December 20, 2017 (Wed)     

Time       :   16:00 - 17:00  

Venue    :  1F Conference Room, Institute of Molecular Embryology and Genetics (IMEG) 

Speaker : Noriko Satake, M.D.

                 Associate Professor, Department of Pediatrics, Comprehensive Cancer Center,

                 University of California, Davis

"Beyond chemotherapy : Targeting cancer and cancer stem cells"

Leukemia stem cells (LSCs) are the root of cancer and are responsible for treatment resistance and disease relapse.  However, LSCs have not been identified in acute lymphoblastic leukemia (ALL), the most common cancer in children.  Recently, our group discovered a method to identify and isolate LSCs from primary ALL samples.  We demonstrated that the LSCs isolated using our marker have in vivo leukemia-initiating capability and distinct transcriptome profiles.  We have identified 1,135 genes that are differentially expressed between LSCs and the counterpart of LSCs, non-LSCs (p < 0.05).  Of these, 315 genes are upregulated in LSCs.   

The goal of our project is to identify the gene(s) that regulate the "stemness" of LSCs in ALL.  Currently, we are focusing on B-cell type ALL (B-ALL), the most common ALL in children.  We will identify the genes which are important for LSC maintenance using an in vivo shRNA screening method and leukemia xenograft models with cell lines and primary leukemia samples. If successful, this project could have a significant impact on the most important challenges in cancer treatment : resistance or recurrence of disease.

I will discuss the regulatory mechanisms of myeloid cell development through our research on IRF8, which promotes the differentiation of mononuclear phagocytes (monocytes and dendritic cells), while limiting neutrophil differentiation. The topics will include our unpublished results such as enhancer landscape dynamics revealed by ChIP-seq and the mechanism of early uni-lineage commitment revealed by single cell RNA-seq. 

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