ZHAO Dongxin
Principal Investigator
Drug Discovery and Design Center (DDDC); SIMM Bioinformatics Platform
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CONTACT
zhaodongxin@simm.ac.cn
201203
555 Zu Chong Zhi Road, Zhang Jiang Hi-Tech Park, Pudong, Shanghai, P.R.China
Biography
ZHAO Dongxin, Ph.D., Principal Investigator of Shanghai Institute of Materia Medica, Chinese Academy of Sciences. Dr. Zhao was a Principal Scientist in the Oncology R&D research unit at Pfizer Inc., San Diego site, where she worked on identification of novel cancer therapeutic targets. Before joining Pfizer, Dr. ZHAO completed her postdoctoral research in the Department of Bioengineering at University of California, San Diego and carried out her PhD in Cell Biology at Peking University. Her current research focuses on revealing principles of genetic rewiring during cancer development and treatment response. She develops novel approaches for mapping genotype to phenotype associations with unprecedented precision and depth to guide precision targeting of cancer vulnerabilities and designing new therapeutic interventions.
Education
2004.09 - 2010.01 Ph.D. in Cell Biology, Peking University
2000.09 – 2004.06 B.S. in Biological Sciences, Peking University
Work Experience
2021.02 – Present Principal Investigator, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
2017.12 – 2021.01 Principal Scientist, Oncology R&D, Pfizer Inc.
2014.12 – 2017.12 Postdoctoral Scholar, Department of Bioengineering, University of California, San Diego
2013.12 – 2014.12 Postdoctoral Research Associate, Salk Institute for Biological Studies
Research Directions
1. Development and application of high throughput functional genomics technologies.
2. Revealing principles of genetic rewiring during cancer development and treatment response for identification of novel cancer therapeutic targets.
Grants & Research Projects
Achievements
1. Nominated several novel cancer drug targets via integrative analysis of a ranger of functional genomics datasets. Supported project transitions from target validation to the hit-to-lead phase.
2. Systematically dissected cancer genetic interaction maps utilizing an innovative combinatorial CRISPR screening approach (Nature Methods, 2017).
3. Revealed critical redox control points dependent on the KEAP1-NRF2 regulatory axis via combinatorial CRISPR-Cas9 metabolic screens (Molecular Cell, 2018).
4. Discovered the activation of PROX1 and HNF6 in parallel of fate determination pathways promoting metabolic maturation of hepatic cells differentiated from human pluripotent stem cells (Cell Research, 2013).
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Social Titles
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Awards & Honors
1. Pfizer Worldwide Research, Development and Medical Individual Achievement Award, 2020
2. International Society for Stem Cell Research Annual Meeting Travel Award, 2016
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Publications
Selected Publications
1.Zhao D*, Badur MG*, Luebeck J, Maga?a JH, Birmingham A, Sasik R, Ahn CS, Ideker T, Metallo CM, Mali P. Combinatorial CRISPR-Cas9 metabolic screens reveal critical redox control points dependent on the Keap1-Nrf2 regulatory axis. Molecular Cell, 2018 Feb 15
2.Shen JP*, Zhao D*, Sasik R*, Luebeck J, Birmingham A, Bojorquez-Gomez A, Licon K, Klepper K, Pekin D, Beckett AN, Sanchez KS, Thomas A, Kuo CC, Du D, Roguev A, Lewis NE, Chang AN, Kreisberg JF, Krogan N, Qi L, Ideker T, Mali P. Combinatorial CRISPR-Cas9 screens for de novo mapping of genetic interactions. Nature Methods. 2017 Jun;14(6):573-576. (*: co-first author)
3.Zhao D*, Chen S*, Duo S, Xiang C, Jia J, Guo M, Lai W, Lu S, Deng H. Promotion of the efficient metabolic maturation of human pluripotent stem cell-derived hepatocytes by correcting specification defects. Cell Research. 2013 Jan;23(1):157-61.
4.McDonald D, Wu Y, Dailamy A, Tat J, Parekh U, Zhao D, Hu M, Tipps A, Zhang K, Mali P. Defining the teratoma as a model for multi-lineage human development. Cell. 2020 Nov 25;183(5):1402-1419.e18.
5.Parekh U, Wu Y, Zhao D, Worlikar A, Shah N, Zhang K, Mali P. Mapping cellular reprogramming via pooled overexpression screens with Paired Fitness and Single Cell RNA-Sequencing Readout. Cell Systems. 2018 Nov 28;7(5):548-555.e8.
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