闵军霞

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闵军霞   教授

肿瘤生物学博士 博士生导师

浙江大学转化医学研究院及浙江大学附属第一医院

2014年入选浙江省海外引进高层次浙江省千人创新学者

 

个人简历:

 

2002-2006 肿瘤生物学博士 美国密苏里哥伦比亚大学;

2006-2010 博士后 美国哈佛大学医学院;

2010-2014 诺华肿瘤制药团队负责人、新药研发课题组长及博士后导师;

2014 教授、博士生导师 浙江大学转化医学研究院及附属第一医院

 

主要研究方向:以中国高发肿瘤的病人基因组学大数据为出发点,探索适用于中国肿瘤病人基因型的有效新型靶向治疗、免疫治疗及克服靶向耐药的综合治疗策略。

 

主要成就:多年来在美国从事肿瘤转化医学研究,在国际上首先发现鞘氨醇-1-磷酸醇(S1P)代谢通路与肿瘤化疗药物抗性关联及作用靶点;通过运用多种生物模型,系统性阐明了癌基因EZH2通过抑制抑癌基因DAB2IP,进而激活RasNF-kappa B致癌通路诱发并促使肿瘤转移的新机制,为前列腺癌诊治提供了新策略;成功领导8个肿瘤新药研发项目,研究并建立了可预测癌症化合物敏感性和预测驱动基因及通路的新型驱动网络模型;参与领导新型个体化免疫治疗,如CART19B细胞恶性肿瘤。在国际著名杂志包括Nature MedicinePNASMolecularCancer Research等发表数篇原创性论文。多次受邀在国内外做大会学术报告。先后获得包括诺华科技创新奖、诺华肿瘤药物研发最佳业绩奖等一系列奖项。

 

获得的重要奖项

 

2015年长三角绿色制药协同创新中心特聘研究员

2014年浙江省海外高层次人才引进计划浙江省特聘专家

2013 年诺华优秀课题负责人奖

2012 年诺华优秀课题负责人奖

2012 年荣获诺华科技创新奖

2011 年诺华肿瘤药物研发最佳业绩奖

2006 年美国密苏里哥伦比亚大学优秀研究一等奖

 

3)国际学术会议

201586-82015中国器官移植大会暨第二届中国器官移植医师年会

特邀大会报告:基于大数据的免疫细胞干预在器官移植中的转化医学研究(中国武汉)

 

 

2015522-23, International Conference on Interdisciplinary Research on Long-term Care and Healthy Aging

特邀大会报告:Hallmarks of Interconnected Aging with Cancer(中国杭州)

2014 11 30 -12 5 日第七届亚洲无机化学会议The 7th AsBIC7 Conference

特邀大会报告:Roadmap of Deregulated Iron Metabolic Pathways in Cancer

2014 6 22-23 日第五届中美转化医学年会The 5th Sino-American Symposium on

Clinical and Translational Medicine (中国北京)

特邀大会报告:Translational Medicine at the Zhejiang University

2014 6 20-21 第四届癌症系统生物学国际研讨会 The Fourth International

Workshop on Cancer Systems Biology (ICSB 2014) (中国吉林)

特邀大会报告:The power of network analysis in discovering novel cancer therapeutics

2014 3 09-14 , Keystone Symposia: Inflammation, Infection and Cancer joint with the

conference on Immune Evolution in Cancer (加拿大)

Poster presentation “Identification of Tumor-Specific Splicing Isoforms in TCGA”

2013 4 21- 26 Gordon Research Conference, Cancer Genetics and Epigenetics (意大利)

Poster presentation “DNA methylation analysis of triple-negative breast cancer”

2008 5 27-29 , Harvard Medical School Genetics Department Retreat (美国)

大会报告 “Identifying a novel oncogenes-tumor suppressor pathway in cancer

metastasis”

2008 1 11 日,MIT & DF/HCC Ludwig Center Retreat (美国)

Poster presentation “A novel tumor suppressor in prostate cancer tumorigenesis &

metastasis”

2007 10 10-12 Colrain 20th Anniversary Meeting (美国)

大会报告“A novel tumor suppressor in prostate cancer tumorigenesis & metastasis”

2005 4 EB Annual Meeting San Diego, CA (美国)

Poster Presentation “Sphingosine-1-phosphate metabolic enzymes affect the cellular

response to chemotherapeutic drugs in a p38 dependent manner”

 

4)主要论著(Selected Publications *Corresponding author)

1.    An P, Zhou D, Wang H, Wu Q, Guo X, Wu A, Zhang Z, Zhang D, Xu X, Mao Q, Shen X, Zhang L, Xiong Z, He L, Min J*, Liu Y* and Wang F*. Elevated serum transaminase activities were associated with increased serum levels of iron regulatory hormone hepcidin and hyperferritinemia risk. Scientific Reports, 2015, Aug 20; 5:13106. * co-corresponding author

2.    Fang XF, Wang H, An P, Min J, and Wang F*. Cardiomyocyte-specific deletion of ferroportin using MCK-Cre has no apparent effect on either cardiac iron homeostasis. International Journal of Cardiology, 2015 Jul 31; 201:90-92.

3.    Mu M, An P, Shen X, Wu Qian, Shao D, Wang H, Zhang Y, Zhang S, Yao H, Min J*, Wang F*. The dietary flavonoid myricetin regulates iron homeostasis by suppressing hepcidin expression. Journal of Nutritional Biochemistry. 2015, accepted. * co-corresponding author

4.    Zhou Q., Derti A., Ruddy D., Rakiec D., Kao I., Lira M, Gibaja V, Chan H, Yang Y, Min J, Schlabach M, Stegmeier F. A chemical genetics approach for the functional assessment of novel cancer genes. Cancer Research. 2015.

5.   Wu Q, Wang H, An P, Tao Y, Deng J, Zhang Z, Shen Y, Min J*, Wang F*. HJV and HFE Play Distinct Roles in Regulating Hepcidin. Antioxidants & Redox Signaling, 2015, Jan 21 [Epub ahead of print]* co-corresponding author

6.   Huang T#, Lan L#, Fang X, An P, Min J, Wang F*. Promises and Challenges of Big Data Computing in Health Sciences. Big Data Research, 2015, in press (Invited review)

7.    Wang Y, Lee YM, Baitsch L, Huang A, Xiang Y, Tong H, Lako A, Von T, Choi C, Lim E, Min J, Li L, Stegmeier F, Schlegel R, Eck MJ, Gray NS, Mitchison TJ, Zhao J. MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells. eLife. 2014 May 20;3:e01763. doi: 10.7554/eLife.01763.

8.    Jaeger S, Min J, Nigsch F, Camargo M, Hutz, J, Cornett A, Cleaver S, Buckler A, Jenkins JL. Causal Network Models for Predicting Compound Targets and Driving Pathways in Cancer. J Biomol Screen. 2014 Feb 11;19(5):791-802 (co-first author)

9.   Min J, Zaslavsky A, Fedele G, McLaughlin SK, Reczek EE, De Raedt T, Guney I, Strochlic DE, Macconaill LE, Beroukhim R, Bronson RT, Ryeom S, Hahn WC, Loda M, Cichowski K. An oncogene-tumor suppressor cascade drives metastatic prostate cancer by coordinately activating Ras and nuclear factor-kappaB. Nature Medicine. 2010 Mar;16(3):286-94.

10.  Sridevi P, Alexander H, Laviad EL, Min J, Mesika A, Hannink M, Futerman AH, Alexander S. Stress-induced ER to Golgi translocation of ceramide synthase 1 is dependent on proteasomal processing. Experimental Cell Research. 2010 Jan 1;316(1):78-91.

11. Van Driessche N, Alexander H, Min J, Kuspa A, Alexander S, Shaulsky G. Global transcriptional responses to cisplatin in Dictyosteliumdiscoideum identify potential drug targets. Proc Natl Acad Sci U S A. 2007 Sep 25;104 (39):15406-11.

12.  Min J, Mesika A, Sivaguru M, Van Veldhoven PP, Alexander H, Futerman AH, Alexander S. (Dihydro)ceramide synthase 1 regulated sensitivity to cisplatin is associated with the activation of p38 mitogen-activated protein kinase and is abrogated by sphingosine kinase 1. Molecular Cancer Research. 2007 Aug;5(8):801-12

13.  Min J, Sridevi P, Alexander S, Alexander H. Sensitive cell viability assay for use in drug screens and for studying the mechanism of action of drugs in Dictyosteliumdiscoideum. Biotechniques. 2006 Nov;41(5):591-5

14. Alexander S, Min J, Alexander H. Dictyosteliumdiscoideum to human cells: pharmacogenetic studies demonstrate a role for sphingolipids in chemoresistance. Biochim Biophys Acta. 2006 Mar;1760(3):301-9.

15. Min J, Van Veldhoven PP, Zhang L, Hanigan MH, Alexander H, Alexander S. Sphingosine-1-phosphate lyase regulates sensitivity of human cells to select chemotherapy drugs in a p38-dependent manner. Molecular Cancer Research. 2005 May;3(5):287-96

16. Min J, Traynor D., Stegner A.L, Zhang L., Hanigan M.H., Alexander H., and Alexander S. Sphingosine kinase regulates the sensitivity of DictyosteliumDiscoideumcells to the anticancer drug cisplatin. Eukaryotic Cell, 2005;4:178-189

17. Min J, Stegner A.L, Alexander H. and Alexander S. Overexpression of sphingosine-1-phosphate lyase or inhibition of sphingosine kinase in Dictyostelium discoideum results in a selective increase in sensitivity to platinum based chemotherapy drugs. Eukaryotic Cell, 2004;3:795-805

Junxia MinPhD

Professor

Institute ofTranslational Medicine

Zhejiang University

79 QingchunRd, Hangzhou, Zhejiang

310058China

Email:junxiamin@zju.edu.cn

 

Dr. Junxia Mincurrentlyserves asa professorat Institute of Translational Medicine,Zhejiang University, Hangzhou, China.Her researchinterest is mainly focused on three areas: 1. to explore novel therapeutics, including molecular targeted therapy andimmunotherapy, for gastrointestinal cancer; 2. to elucidate molecular mechanisms of resistance to targeted cancer therapeutics; 3.to furtherrefine our previously established causal network models for realizably predicting drug sensitivity and defining driving pathways in Chinese-prevalent cancer types.

Dr. Min earned herPh.D. from University of Missouri-Columbia in 2006. During her 4 year-Ph.D. training period, she published 7 peer-reviewed research articles. Her key finding wasdiscovered anddefinedthe importantroles of sphingolipid metabolic pathway in resistanceto platinum-based anticancer drugs. Her findingsopened new avenue for targeting sphingolipid metabolic pathway in cancer therapeutics. In 2006, Dr. Min went to Harvard Medical School, where shespent over 4.5 years for her postdoctoral training at the Department of Medicine, Brigham and Women’s Hospital. Her major scientific achievement was identification and functional characterization of EZH2/DAB2IP as oncogene-tumor suppressor cascade in promoting prostate cancer tumorigenesis and progression. The finding was highlighted as the breakthrough of year 2010 in prostate cancer research and on The Wall Street Journalhttp://online.wsj.com/news/articles/SB10001424052748703279704575334982806405218.

Since 2010, Dr. Min joined Novartisas a research investigator/postdoc mentor at Cambridge, U.S.A. Using integrative meta-analysis in conjunction with functional screens, Dr. Min's groupfocused on target identification and validation.For tumor suppressor genes, such as p53, Min groupwas strived to identify critical synthetic lethal nodes by employing large-scale RNAi screening.In addition, Dr. Minisalso interested in understanding molecular mechanisms of resistance in response to targeted therapies.

Research Interest

Novel Target Discovery: Molecularly targeted cancer therapies are designed to specifically block the driving ‘oncogenes’ that sustain tumorigenesis and tumor progression while sparing normal cells. Gleevec, which targets BCR-ABL in CML, was one of the first demonstrations of this new paradigm of cancer treatment, and has clinically been proven to be more effective and less toxic than chemotherapies. To discover novel cancer therapeutic targets, our laboratory is focusing on applying integrative genomic and functional approaches. For tumor suppressor genes, such as p53, we aim to discover critical synthetic lethal nodes by employing large-scale RNAi screening. Synthetic lethal nodes are defined as genes that only become essential in the context of another mutation. Thus, it is expected that targeting synthetic lethal genes of key cancer pathways would provide wider therapeutic windows compared to cytotoxic chemotherapeutics.

Cancer Immunotherapy: It refers a strategy that harnesses the body's immune system to combat tumors. With remarkable durable-response, cancer immunotherapy was selected as the breakthrough of the Year for 2013. The recent successful story of immune-checkpoint blockade ipilimumab (Yervoy) for melanoma, and novel chimeric T cell therapy-CART19 for CLL and ALL patients, have raised hope that immunotherapy may provide oncologists new options for treatment in the future. By using what we have learned about the immune system, we aim to explore effective immunotherapeutic target for Chinese-prevalent cancer types.

Molecular Mechanisms of Resistance: In addition, we are interested in understanding mechanisms of resistance in response to cancer therapies, in particular mechanisms that circumvent response to targeted therapies. We are using primary xenograft models (PTX) to study the causal genes or pathways that account for the resistance to targeted therapies.

Cancer Network Metadata Analysis: Another area of research interest is to discover novel therapeutic approaches for cancers that currently lack of targeted therapy, such as triple-negative breast cancer (TNBC). Using network analysis in couple with genomic and epigenetic profiling data mining, we aim to define driving pathways in molecularly defined subtypes of Asian prevalent cancer.

 

 

 

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