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Faculty

Members of CAS, CAE
National Outstanding Young Scientists Award
Principal Investigators
 
Address: 320 Yue Yang Road, Shanghai 200031, P.R. China
Tel: 86-21-54920000
Fax: 86-21-54921011
Email: sibcb@sibs.ac.cn
Website: www.sibcb.ac.cn
 
Principal Investigators
 
JIANG Hai
Ph.D., Professor
Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue-yang Road,
Shanghai 200031, China.
Email: hai@@sibcb.ac.cn

Research Areas
Genetic determinants of drug sensitivity; Cancer genomics; Novel oncogenes and tumor suppressors; Novel regulators of major signaling pathways;

Research Interests

1) Drug efficacy. Improving treatment efficacy is a major challenge for healthcare and biomedical research. With the rapidly improving understanding of the genomes and expression landscapes of human populations as well as those of cancer samples, significant opportunities lie in the rational design of personalized medicine that can maximally benefit individual patients. Using a high-performance screen system, we can apply genome-wide CRISPR screen techniques to systematically identify novel genetic events that cause resistance or hypersensitivity to more than 30 types of anticancer drugs. Such a platform can also be extended to immunosuppressants, antivirals, cholesterol-lowering drugs and other types of medicines, yielding new insights into their pharmacogenomics, as well as novel genes involved in the pathways modulated by these drugs.
2) Novel oncogenes and tumor suppressors. Our group also study cancer genomes to identify novel cancer genes. Such efforts are based on analysis of the large number of cancer genomes deposited in common cancer database such as COSMIC. For example, we showed that based on the type of nucleotide changes and the sequences surrounding mutation sites, at nucleotide level different types of mutations are generated at tendencies that can vary by up to 400 folds. This means certain types of cancer-promoting mutations will only be observed in a small number of samples in cancer database, due to the high unlikeliness of generating the underlying nucleotide mutations. By factoring the ^relative mutational difficulty ̄ back in, we can pick up such kind of rare but cancer promoting mutations from the background. This leads to the discovery of potential cancer-promoting roles for many genes previously unnoticed in the cancer field. We also studied gene amplification & deletion status of more than 14,000 cancer samples, generating a high-resolution cancer gene amplification & deletion map, which indicated several novel oncogenes and tumor suppressors. We are currently studying candidate novel cancer genes identified by the above approaches.

3) Novel regulators of major signaling pathways. Cancer and many other types of diseases are caused by deregulation of major signaling pathways. We developed a platform that can rapidly test whether a candidate event alters any of 15 major signaling pathways, providing an efficient platform to deconvolute the mechanism of novel oncogenes and tumor suppressors, as well as for genes implicated in various types of inherited diseases. Such a platform can also efficiently employ genome-wide screen techniques to uncover novel components of major signaling pathways, which will lead to better understanding of human diseases and potentially novel drug targets.

Selected Publications

  1.  Xu L, Li P, Hao X, Lu Y, Liu M, Song W, Shan L, Yu J, Ding H, Chen S, Yang A, Zeng YA, Zhang L*, Jiang H*. SHANK2 is a frequently amplified oncogene with evolutionarily conserved roles in regulating Hippo signaling. (2020) Protein & Cell (*Corresponding author) (In press)
  2. Shan L, Yu J, He Z, Chen S, Liu M, Ding H, Xu L, Zhao J, Yang A, Jiang H. Defining relative mutational difficulty to understand cancer formation. (2020) Cell Discovery (In press)
  3. Jiang H. The Expanding Vulnerabilities of Being UTXless. Signal transduction and targeted therapy (2019) 4:12.
  4. Ding H, Zhao J, Zhang Y, Yu J, Liu M, Li X, Xu L, Lin M, Liu C, He Z, Chen S, Jiang H. Systematic analysis of drug vulnerabilities conferred by tumor suppressor loss. (2019) Cell Reports 27,3331-3344. (Recommended by Faculty of 1000)
  5. Li X, Zhang Y, Zheng L, Liu M, Chen CD, Jiang H. UTX is an escape from X-inactivation tumor-suppressor in B cell lymphoma. (2018) Nature Communications. 9(1):2720
  6. Liu C, Ding H, Li X, Pallasch CP, Hong L, Guo D, Chen Y, Wang D, Wang W, Wang Y*, Hemann MT*, Jiang H*. A DNA/HDAC dual-targeting drug with significantly enhanced anticancer potency. (2015) EMBO Molecular Medicine, 7(4):438-49 (*Corresponding author)
  7. Wang N, Ding H, Liu H, Li X, Wei L, Yu J, Liu M, Ying M, Gao W, Jiang H*, Wang Y*. A novel recurrent CHEK2 Y390C mutation identified in high risk Chinese breast cancer patients impairs its activity and is associated with increased breast cancer risk. (2015) Oncogene, 34(40):5198-205 (*Corresponding author)
  8. Wu J#, Jiang H#, Luo S#, Zhang M, Zhang Y, Sun F, Huang S and Li H. Caspase-mediated cleavage of C53/LZAP protein causes abnormal microtubule bundling and rupture of the nuclear envelope. (2013) Cell Research, 23(5):691-704. (#equal contribution)
  9. Jiang H, Pritchard JR, Williams RT, Lauffenburger DA, Hemann MT. A mammalian functional-genetic approach to characterizing cancer therapeutics. (2011) Nature Chemical Biology. 7(2):92-100.
  10. Reinhardt HC#, Jiang H#, Hemann MT and Yaffe MB. Exploiting synthetic lethal interactions for targeted cancer therapy. (2009) Cell Cycle 8(19) :3112-9. (#equal contribution)
  11. Jiang H#, Reinhardt HC#, Bartkova J, Tommiska J, Blomqvist C, Nevanlinna H, Bartek J, Yaffe MB, Hemann MT. The combined status of ATM and p53 link tumor development with therapeutic response. (2009) Genes Dev. 23(16):1895-909. (#equal contribution) (Recommended by Faculty of 1000)
  12. Jiang H#, Wu J#He C, Yang W, Li H. Tumor suppressor protein C53 antagonizes checkpoint kinases to promote cyclin-dependent kinase 1 activation. (2009) Cell Research. 19(4):458-68. (#equal contribution)
  13. Jiang H, Luo S, Li H. Cdk5 activator-binding protein C53 regulates apoptosis induced by genotoxic stress via modulating the G2/M DNA damage checkpoint. (2005) Journal of Biological Chemistry. 280(21):20651-9

Education Background & Academic Experience
From 2011, Principle Investigator, Shanghai Institute of Biochemistry and Cell Biology (SIBCB), CAS, Shanghai, China.
2007-2011, Postdoctoral Associate, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
2000-2006, Doctor of Philosophy, the Integrated Graduate Program (Cancer / Cell Biology), Northwestern University, the Feinberg School of Medicine
1996-2000, Bachelor of Science, Department of Biotechnology, Peking University, Beijing, China

Research Team

 

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