Bio

Professional Education


  • Doctor of Philosophy, Harbin Medical University (2010)
  • Bachelor of Medicine, Unlisted University (2010)
  • Doctor of Philosophy, Unlisted University (2010)

Stanford Advisors


Publications

Journal Articles


  • Differential expression and functions of microRNAs in liver transplantation and potential use as non-invasive biomarkers. Transplant immunology Wei, L., Gong, X., Martinez, O. M., Krams, S. M. 2013; 29 (1-4): 123-129

    Abstract

    MicroRNAs (miRNAs) are important regulators in many biologic processes and have been implicated in the control of genes relevant to acute rejection and liver functions. Here we review the miRNAs specifically expressed in allografts during acute rejection and discuss potential roles for these miRNAs in liver dysfunction. We focus on miRNAs dysregulated both in the liver and in peripheral blood mononuclear cells and include a discussion of the potential for these miRNAs as non-invasive biomarkers to reflect liver status posttransplant.

    View details for DOI 10.1016/j.trim.2013.08.005

    View details for PubMedID 24001411

  • Modulating the Strength and Threshold of NOTCH Oncogenic Signals by mir-181a-1/b-1 PLOS GENETICS Fragoso, R., Mao, T., Wang, S., Schaffert, S., Gong, X., Yue, S., Luong, R., Min, H., Yashiro-Ohtani, Y., Davis, M., Pear, W., Chen, C. 2012; 8 (8)

    Abstract

    Oncogenes, which are essential for tumor initiation, development, and maintenance, are valuable targets for cancer therapy. However, it remains a challenge to effectively inhibit oncogene activity by targeting their downstream pathways without causing significant toxicity to normal tissues. Here we show that deletion of mir-181a-1/b-1 expression inhibits the development of Notch1 oncogene-induced T cell acute lymphoblastic leukemia (T-ALL). mir-181a-1/b-1 controls the strength and threshold of Notch activity in tumorigenesis in part by dampening multiple negative feedback regulators downstream of NOTCH and pre-T cell receptor (TCR) signaling pathways. Importantly, although Notch oncogenes utilize normal thymic progenitor cell genetic programs for tumor transformation, comparative analyses of mir-181a-1/b-1 function in normal thymocyte and tumor development demonstrate that mir-181a-1/b-1 can be specifically targeted to inhibit tumor development with little toxicity to normal development. Finally, we demonstrate that mir-181a-1/b-1, but not mir-181a-2b-2 and mir-181-c/d, controls the development of normal thymic T cells and leukemia cells. Together, these results illustrate that NOTCH oncogene activity in tumor development can be selectively inhibited by targeting the molecular networks controlled by mir-181a-1/b-1.

    View details for DOI 10.1371/journal.pgen.1002855

    View details for Web of Science ID 000308529300016

    View details for PubMedID 22916024

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