演讲嘉宾--应颂敏

应颂敏
应颂敏
研究学习经历:

应颂敏,先后留学英国、德国,分别在谢菲尔德大学获得硕士学位,慕尼黑工业大学获得博士学位,并在牛津大学做了6年的博士后研究工作。浙江大学教授、博士生导师,国家优秀青年科学基金获得者,中组部“青年千人计划”入选者,中华医学会呼吸病学分会青年委员会副主任委员、哮喘学组秘书,国家“青年千人计划”专家生物医药小组副组长,浙江省“千人计划”特聘专家,浙江省杰出青年科学基金获得者。一直致力于慢性气道炎症和呼吸系统肿瘤中基因组稳定性的分子调控机制和靶向治疗的研究,注重基础医学与临床医学相结合,逐渐在这些领域形成了具有特色和影响力的系统性研究体系。主持多项国家自然科学基金优青项目、面上项目、中组部青年千人项目、科技部973项目子课题和国家重点研发计划项目子课题等。发表SCI论文38篇,总影响因子约270分。其中以第一或通讯作者(含共同)在国际权威学术期刊Nature(2015)、Nature Cell Biology(2013)、Cancer Research(2012、2016)、Nucleic Acids Research(2009)、Journal of Infectious Diseases(2008)、International Journal of Cancer(2014)、Carcinogenesis(2013)、Oncotarget(2015、2016a、2016b)等发表SCI论文20篇。4篇论文被Faculty of 1000推荐。其主要成果被Nature、Science、Cell、Nature Reviews Cancer、Nature Reviews Drug Discovery、Nature Reviews Genetics、Nature Reviews Molecular Cell Biology、Nature Cell Biology、Nature Structural & Molecular Biology、Cell Stem Cell、Molecular Cell、Developmental Cell等杂志引用超过1000次,受到国际同行广泛关注。受邀担任英国肺脏基金会(British Lung Foundation)和丹麦独立研究委员会(Danish Council for Independent Research)项目评审专家,The Clinical Respiratory Journal杂志编委。

近期发表论文:
    1.    Oleandrin Induces DNA Damage Responses in Cancer Cells by Suppressing the expression of Rad51, Bao Z, Tian B, Wang X, Feng H, Liang Y, Chen Z, Li W, Shen H and Ying S*, Oncotarget. 2016 in press (*通讯作者) IF:5.008
    2.    Activation of mTOR in pulmonary epithelium promotes LPS-induced acute lung injury, Hu Y, Lou J, Mao YY, Lai TW, Liu LY, Zhu C, Zhang C, Liu J, Li YY, Zhang F, Li W, Ying SM, Chen ZH and Shen HH*, Autophagy. 2016 in press IF:9.108
    3.    DNA-PKcs and PARP1 bind to unresected stalled DNA replication forks where they recruit XRCC1 to mediate repair, Ying S*, Chen Z, Medhurst AL, Neal JA, Bao Z, Mortusewicz O, McGouran J, Song X, Shen H, Hamdy FC, Kessler BM, Meek K and Helleday T*, Cancer Res. 2016 Mar 1;76(5):1078-88. (*通讯作者) IF:9.329
    4.    Effectiveness and Safety of Poly (ADP-ribose) Polymerase Inhibitors in Cancer Therapy: A Systematic Review and Meta-analysis, Bao Z, Cao C, Geng X, Tian B, Wu Y, Zhang C, Chen Z, Li W, Shen H*, Ying S*,  Oncotarget. 2016 Feb 16;7(7):7629-39. (*通讯作者) IF:6.359
    5.    Autophagy Is Essential for Ultrafine Particle-Induced Inflammation and Mucus Hyperproduction in Airway Epithelium, Chen ZH, Wu YF, Wang PL, Wu YP, Li ZY, Zhao Y, Zhou JS, Zhu C, Cao C, Mao YY, Xu F, Wang BB, Cormier SA, Ying SM, Li W, Shen HH, Autophagy. 2016 Feb;12(2):297-311. IF: 11.753
    6.    Replication stress activates DNA repair synthesis in mitosis, Minocherhomji S#, Ying S# (#共同第一作者), Bjerregaard VA, Bursomanno S, Aleliunaite A, Wu W, Mankouri HW, Shen H, Liu Y, Hickson ID, Nature. 2015 Dec 10;528(7581):286-90. (Recommended by Faculty of 1000; Comment in: DNA repair: The cell cycle flavours of repair. [Nat Rev Mol Cell Biol. 2016][Nat Rev Genet. 2016]) IF:41.456
    7.    Acute MUS81 depletion leads to replication fork slowing and a constitutive DNA damage response, Xing M, Wang X, Palmai-Pallag T, Shen H, Helleday T, Hickson ID, Ying S*,  Oncotarget. 2015 Nov 10;6(35):37638-46. (*通讯作者) IF:6.359
    8.    Inhibiting WEE1 selectively kills histone H3K36me3-deficient cancers by dNTP starvation, Pfister SX, Markkanen E, Jiang Y, Sarkar S, Woodcock M, Pai CC, Zalmas LP, Orlando G, Mavrommati I, Drobnitzky N, Dianov GL, Verrill C, Macaulay V, Ying S, La Thangue NB, D'Angiolella V, Ryan A, Humphrey TC, Cancer Cell. 2015 Nov 9; 28(5): 557–568. (Comment in: Epigenetic Deficiencies and Replicative Stress: Driving Cancer Cells to an Early Grave. [Cancer Cell. 2015]) IF:23.523
    9.    Esophageal intraepithelial invasion of Helicobacter pylori correlates with atypical hyperplasia, Li W, Tian D, Guan X, Yun H, Wang H, Xiao Y, Bi C, Ying S* and Su M*, Int J Cancer. 2014 Jun 1;134(11):2626-32. (*通讯作者) IF:5.085
    10.  MUS81 promotes common fragile site expression, Ying S*, Minocherhomji S, Chan KL, Palmai-Pallag T, Chu WK, Wass T, Mankouri HW, Liu Y, Hickson ID*, Nat Cell Biol. 2013 Aug;15(8):1001-7. (*通讯作者) (Recommended by Faculty of 1000; Comment in: A blooming resolvase at chromosomal fragile sites. [Nat Cell Biol. 2013]) IF:19.679
    11.  DNA damage response in peritumoral regions of oesophageal cancer microenvironment, He H, Tian D, Guo J, Liu M, Chen Z, Hamdy FC, Helleday T, Su M*, Ying S*, Carcinogenesis. 2013 Jan;34(1):139-45. (*通讯作者) IF:5.334
    12.  Mre11-dependent degradation of stalled DNA replication forks is prevented by BRCA2 and PARP1, Ying S, Hamdy FC, Helleday T, Cancer Res. 2012 Jun 1;72(11):2814-21. (Recommended by Faculty of 1000) IF:9.329
    13.  BRCA2 dependent homologous recombination is required for repair of Arsenite-induced replication lesions in mammalian cells, Ying S, Myers K, Bttomley S, Helleday T, Bryant HE, Nucleic Acids Res.2009 Aug;37(15):5105-13. IF:9.112
    14.  Replication stress induces sister-chromatid bridging at fragile site loci in mitosis, Chan KL, Palmai-Pallag T, Ying S, Hickson ID, Nat Cell Biol. 2009 Jun;11(6):753-60. (Recommended by Faculty of 1000) IF:19.679
    15.  Premature apoptosis of Chlamydia-infected cells disrupts chlamydial development, Ying S, Pettengill M, Latham ER, Walch A, Ojcius DM, Häcker G, J Infect Dis. 2008 Nov 15;198(10):1536-44. IF:5.997
会议报告摘要:
Targeting replication stress in cancer cells for cancer therapy(4月23日,13:30 - 13:55 pm)

Oncogene-induced DNA replication stress has been implicated as a driver of tumorigenesis. Many chromosomal rearrangements characteristic of human cancers originate from specific regions of the genome called common fragile sites (CFSs). CFSs are difficult-to-replicate loci that manifest as gaps or breaks on metaphase chromosomes (termed CFS 'expression'), particularly when cells have been exposed to replicative stress. Replication stress is repaired via multiple signaling pathways. Silencing of two or more complementary signaling pathways can lead to cell death, while loss of any single genetic function does not show a severe phenotype because of backup solutions. This kind of interaction between two or more genes is coined 'synthetic lethality'. In this talk, we are going to discuss how replication stress can be resolved in cancer cells, as well as possible potential strategy for targeted therapy.

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第四届肿瘤基础和转化医学前沿国际研讨会