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薛少安

西安文理学院

薛少安,陕西省“百人计划”特聘教授。1999年获伦敦大学帝国理工医学院病毒肿瘤学博士学位,曾先后在世界著名的英国帝国理工学院 (Imperial College London)和伦敦大学学院(University College London)从事博士后、研究讲师及高级讲师工作。现任西安文理学院生物与环境工程学院基因工程实验室主任。

薛少安主要从事EBV在中国鼻咽癌等恶性肿瘤中基因的表达与调控以及转化医学所涉及的肿瘤的免疫基因治疗等基础与应用基础研究。成功地研发出一条利用T细胞受体(TCR)基因转导来获取肿瘤特异性T细胞的新途径。2005年获第34届国际实验血液学会研究新人奖。在SCI期刊发表论文60余篇,其中影响因子高于3分的国际刊物有54篇,高于5分的38篇,高于10分的12篇,高于20分的1篇。发表的文章已在国际公认的科学文献数据库机构Thomson Reuters的网站建立了ISI论文信息库(http://www.researcherid.com/rid/A-2735-2011),共有112篇文章被统计; 共被引用2234次,平均每篇被引用20次;H-index引用指数为28。

由于在肿瘤的TCR免疫基因治疗领域里的突出贡献和影响,薛少安已被欧洲转化医学委员会(EUSTM)聘请为临床微生物与免疫学分会专家组成员(http://eutranslationalmedicine.org/clinical-microbiology-and-immunology/),同时被Journal of Clinical Immunology & Immunotherapy、Journal of Immunotherapy applications、Annals of Vaccine and Immunization、Journal of Hematological Malignancies、American Journal of Leukemia Research、International Journal of Hematology and Therapy、Journal of Translational Clinical and Experimental Oncology以及 Journal of Oncology and Cancer Research 等8家国际杂志聘请为编委。

演讲题目: TCR gene therapy of CMV & EBV associated malignancies.
演讲摘要:Allogeneic SCT is one of the curative strategies for the treatment of human leukaemia. But to prevent graft rejection, patients are profoundly immunosuppressed. Under such conditions, reactivation of CMV & EBV often occur. CMV can cause severe CMV diseases, and has been linked with medulloblastoma. EBV can cause post transplant lymphoproliferative disorder, and is associated with a number of human malignancies, including Burkitt’s lymphoma, Hodgkin’s lymphoma and nasopharyngeal carcinoma. Adoptive transfer of CMV- & EBV-specific CD8+ T cells has proven effective in the treatment of virally associated diseases, but the isolation and expansion of these virus-specific T cells has been labor intensive and technically difficult. In this study, we isolated HLA-A2-restricted TCR genes specific for CMV and EBV, and retrovirally transduced them into human T cells, thus generated MHC class I-restricted both CD8+ and CD4+ T cells specific for CMV and EBV. In vitro studies demonstrated that these CMV and EBV specific T cells can bound HLA-A2/peptide multimers, and produced cytokines when stimulated 36 with tumor cells expressing the relevant viral antigens. Using the xenogeneic NOD/SCID in vivo model, we show that these TCR-engineered T cells efficiently controlled the tumors expressing the TCRrecognized CMV or EBV antigens. Together, we describe a robust approach for generating CD8+ CTL and CD4+ Th cells capable of providing MHC class I-restricted antitumor immunity.
Keywords: Microbiome, fecal microbiota transplant, Irritable Bowel Syndrome (IBS)

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