The University of Texas MD Anderson Cancer Center
Department of Epigenetics and Molecular Carcinogenesis
As an Instructor in the department of Neuro-Oncology, MD Anderson Cancer Center, I have focused my research interest to improve current treatment strategies for glioblastoma (GB) patients. Current treatment cares for glioblastoma patients are tumor resection, radiotherapy, chemotherapy, and recently added TTFields but with that the median survival is still not more than 12 months. To understand the role of the aberrant molecular pathways of GBs in the DNA damage response pathway is a crucial step to solve the recurrence/resistance of GBs to therapies. I have largely focused my research area to understand the biology of GB in response to DNA damage and my research identified a novel mechanism that tyrosine kinase receptor, TIE2, upon radiation translocates to the nucleus and phosphorylates core histone H4 at Tyr51 and recruit ABL1 (cAbl) in the DNA damage site along with other DNA repair proteins to show radioresistance. Our data also find the link between Core Histone phosphorylation and ABL1-mediated DNA repair as inhibition or silencing of ABL1 impedes DNA repair efficiency. We reported our data in Science Advances. I am also involved in some novel projects to find out detail mechanism of radioresistance of glioblastoma, I am also interested to find the genome-wide distribution of TIE2, H4pY51 and PIK3R1 by ChIP-Seq, PIK3R1 was found as reader of H4pY51 in our SH2 protein array and PIK3R1 relation with DNA repair through histone phosphorylation will open a very optimistic treatment strategy for cancer patients.
Education & Training
PhD, Chiba University, Japan, 2008