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肿瘤研究所Ⅰ级PI
http://www.rosunbags.com/       2018-09-28
Ⅰ级PI  陈可欣

  陈可欣,博士,教授,博士生导师,现任天津医科大学肿瘤医院副院长,教育部“常见恶性肿瘤预防的研究”长江学者和创新团队发展计划及滚动支持带头人,国家卫生计生突出贡献中青年专家,天津市特聘教授,天津市“十一五”“十二五”综合投资重点学科带头人,曾荣获天津市“五一”劳动奖章和“天津市优秀回国人员”称号。中国抗癌协会肿瘤流行病学专业会员会副主任委员,天津市预防医学会流行病分会主任委员,天津市吸烟与健康协会理事会副会长,天津医学会临床流行病学专业委会常委,国际肿瘤登记报告协会(IACR)的会员、美国国家肿瘤登记协会会员(NCRA)、中国肿瘤登记报告协会的常务理事;现为《Cancer Medicine》、《Chinese Journal of Cancer》、《中国肿瘤临床》等杂志编委。

  1987年毕业于天津医科大学,获公共卫生学士学位。同年分配到天津市肿瘤医院流行病学研究室,从事肿瘤流行病学研究工作。2003年获硕士学位,2007年获博士学位。2006年2月至2007年5月受国家教委委派在美国M. D. Anderson肿瘤中心做博士后,从事肿瘤分子流行病学研究。

  长期从事肿瘤流行病学研究工作,包括天津恶性肿瘤的流行趋势研究、常见恶性肿瘤的早期筛查和肿瘤分子流行病学的研究。作为肿瘤重点研究方向之一,与所在单位一起成功申请肿瘤国家重点学科、乳腺癌防治教育部重点实验室和创新团队。2006年作为学科带头人获得天津市“十一五”、“十二五”综合投资重点学科,2010年获得中央财政支持地方高校发展专项资金肿瘤流行病重点学科,2011年获得教育部“常见恶性肿瘤预防的研究”创新团队,并于2015年获教育部创新团队滚动支持。

  作为项目负责人主持教育部创新团队发展计划基金及滚动支持项目、国家自然科学基金重大国际(地区)合作与交流项目1项、863专项1项、科技部新药创制平台项目1项、国家自然科学基金3项、省部级基金项目8项、NCI、UICC等国际合作项目10余项。获得9项省部级以上科技进步奖,其中作为第二完成人获得国家科技进步二等奖和天津市科技进步一等奖各一项,作为第一完成人获得天津市科技进步一等奖、三等奖和中国抗癌协会科技一等奖各一项。近5年发表学术论文近百篇,其中SCI论文76篇,影响因子IF>10论文15篇,他引频次1038次,其中第一/通讯作者文章35篇,单篇最高引用频次165次,研究成果发表在Annals of Oncology、 Nature Communications、Hepatology、Cancer Cell、Nature Genetics、J Clinical Invest、PNAS、International Journal of Epidemiology、Clinical Cancer Res、 Carcinogenesis等专业研究的杂志。

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级PI 冯玉梅

  冯玉梅,女,1965年1月出生,博士,研究员,教授,博士生导师,天津市“131”创新型人才第一层次人选。1983-1987年大学本科就读于于南开大学化学系应用化学专业,1987-1990年硕士研究生就读于南开大学分子生物学研究所生物化学专业,自1990年毕业至今在天津医科大学肿瘤医院肿瘤研究所工作,2003年晋升为研究员,2006年兼聘为教授,2007年遴选为博士研究生导师。自2000年至今任生物化学与分子生物学研究室主任,兼任中国抗癌协会肿瘤标志专业委员会委员(第二、三、四、五届),中国抗癌协会乳腺癌专业委员会委员(第四、五届),天津市细胞生物学会理事(第一、二届),《中国肿瘤临床》杂志编委(第四届)。2004-2005年受天津市教委资助于美国The University of Texas M. D. Anderson Cancer Center研修,2006-2009年于天津大学在职攻读博士学位。研究方向为肿瘤分子生物学,致力于乳腺癌转移机制研究和肿瘤基因诊断研究。主持国家自然科学基金面上项目5项、天津市自然科学基金重点项目2项、以及国家“九五”科技攻项目关子课题、国家“863”计划子课题、国家科技支撑计划子课题等;作为第一完成人获天津市自然科学三等奖、天津市科技进步三等奖、天津市卫生局科技成果一等奖、天津医科大学科技成果二等奖各1项;作为通讯作者发表SCI论文20篇,至今他引415次,其中一篇入选全球Top 1% ESI高被引优秀论文;指导博士研究生12名、硕士研究生32名,其中3人获天津医科大学优秀博硕士毕业生、1人获天津医科大学优秀博士论文奖励。

  代表性论文(*为通讯作者)

  1. Wang QS, He R, Yang F, Kang LJ, Li XQ, Fu L, Sun B*, Feng YM*. FOXF2 deficiency permits basal-like breast cancer cells to form lymphangiogenic mimicry by enhancing the response of VEGF-C/VEGFR3 signaling pathway. Cancer Lett. 2018, 420:116-126.

  2. Yu ZH#, Lun SM#, He R#, Tian HP, Huang HJ, Wang QS, Li XQ, Feng YM*. Dual Function of MAZ Mediated by FOXF2 in Basal-like Breast Cancer: Promotion of Proliferation and Suppression of Progression. Cancer Lett. 2017, 402:142-152.

  3. Tan CC#, Li GX#, Tan LD, Du X, Li XQ, He R, Wang QS, Feng YM*. Breast cancer cells obtain an osteomimetic feature via epithelial-mesenchymal transition that has undergone BMP2/RUNX2 signaling pathway induction. Oncotarget. 2016, 7(48):79688-79705.

  4. Li XQ, Lu JT, Tan CC, Wang QS, Feng YM*. RUNX2 promotes breast cancer bone metastasis by increasing integrin α5-mediated colonization. Cancer Lett. 2016;380(1):78-86.

  5. Li XQ, Du X, Li DM, Kong PZ, Sun Y, Liu PF, Wang QS, Feng YM*. ITGBL1 Is a Runx2 Transcriptional Target and Promotes Breast Cancer Bone Metastasis by Activating the TGFβ Signaling Pathway. Cancer Res. 2015, 75(16): 3302-3313.

  6. Cai J, Tian AX, Wang QS, Kong PZ, Du X, Li XQ, Feng YM*. FOXF2 suppresses the FOXC2-mediated epithelial-mesenchymal transition and multidrug resistance of basal-like breast cancer. Cancer Lett. 2015, 367(2):129-37.

  7. Tian HP, Lun SM, Huang HJ, He R, Kong PZ, Wang QS, Li XQ, Feng YM*. DNA Methylation Affects the SP1-regulated Transcription of FOXF2 in Breast Cancer Cells. J Biol Chem. 2015;290(31):19173-83.

  8. Wang QS, Kong PZ, Li XQ, Yang F, Feng YM*. FOXF2 deficiency promotes epithelial-mesenchymal transition and metastasis of basal-like breast cancer. Breast Cancer Res. 2015;17:30.

  9. Yu Y, Xiao CH, Tan LD, Wang QS, Li XQ, Feng YM*. Cancer-associated fibroblasts induce epithelial-mesenchymal transition of breast cancer cells through paracrine TGF-β signalling. Br J Cancer. 2014;110(3):724-732.

  10. Yu Y, Wang XY, Sun L, Wang YL, Wan YF, Li XQ, Feng YM*. Inhibition of KIF22 Suppresses Cancer Cell Proliferation by Delaying Mitotic Exit through Up-regulating CDC25C Expression. Carcinogenesis. 2014;35(6):1416-1425.

  联系电话:022-23340123转6002

  E-mail:fengymei@hotmail.comymfeng@tmu.edu.cn

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级PI  李兵辉

  李兵辉,博士,教授,PI,博士生导师

  教育背景

  2001.09~2006.04理学博士,中国科学院研究生院。专业:生物化学与分子生物学。

  1996.09~2000.07理学学士,江西南昌大学。专业:生物工程。

  工作经历

  2006.05~2007.10博士后(Postdoctoral Fellow),美国西北大学。从事癌症细胞生物学研究。

  2007.11~2010.10研究助理(Research Professional Associate),芝加哥大学。从事癌症与能量代谢方面的研究。

  2010.12~至今教授,天津医科大学附属肿瘤医院肿瘤研究所。

  研究兴趣

  本课题组将着重阐述代谢酶、代谢产物及癌细胞命运之间的关系,以寻找新颖的、特异的抗癌靶点为主要任务!我们的研究兴趣在:

  1、肿瘤生长抑制因子Rb通过控制能量代谢平衡调节细胞转化作用的机制研究。本课题组拟解决Rb是如何控制代谢平衡的及Rb失活的癌细胞是如何控制代谢失衡的,并从中找出能特异杀死Rb失活的癌细胞的分子靶点,为癌症治疗带来新方法、新理念!

  2、研究和代谢相关的脂肪酸合成、蛋白质合成紊乱(ER Stress)及自噬(Autophagy)发生的机制及它们和肿瘤发生发展的关系。

  3、能量代谢如何决定细胞的命运。近些年来,科学家们逐渐意识到几乎所有的细胞信号转导途径最终都汇集在代谢网络上,这迅速催热了癌症的代谢研究。细胞的代谢是如何决定细胞命运的?是如何决定细胞的转化的?我们的研究将着重理清癌细胞中糖代谢、脂代谢及蛋白质代谢之间的关系,寻找癌细胞得以转化的物质基础(代谢本质)。

  4、开发实时生物学功能监测工具。我们将致力于确定研究细胞代谢(决定细胞命运)的方法;将致力于开发实时监测代谢平衡及细胞凋亡的工具。

  Research Description

  In the past decades, most researchers working on cancer were focusing on cell signal transduction, and they made profound progress in understanding and treating cancers. However, cancer still remains a medical challenge and numerous questions remain to be explored. Metabolic and signal systems in cancer cells can be driven by each other, and they are closely connected but remain relatively independent. Altering the signal transduction network absolutely will drive corresponding metabolic changes, however, most researchers usually complete their studies without investigating metabolic changes, because under these conditions the signal transduction system is positive and it promotes the passive metabolism. On the other hand, when we perturb the metabolic network by targeting metabolic enzymes or changing their substrates concentrations, the signal system also will change. In this setting, the positive metabolic system drives passive signal transduction, nonetheless, we can not always figure out how cancer cells die by the rules of typical signal transduction. The metabolic system probably has its own ways to induce cell death.

  Based on our previous studies, we put forward the hypothesis that the irreversible upsetting of metabolic homeostasis can kill cells by some special mechanisms. Cancer cells have many specifically metabolic characteristics that could be rendered as ideal targets for the treatment of cancer. Our future research will be carried out around this hypothesis, and we plan to identify targets to disrupt metabolic homeostasis to kill cancer cells and then dissect their mechanisms.

  Project I: Role of Rb in controlling cell proliferation, growth and transformation via regulating redox balance. We want to know how Rb controls cellular stress, and how Rb regulation of cell proliferation, growth and transformation is related to its ability to control cellular stress. In Rb mutant cancer cells, how is Rb inactivation-induced lethal redox imbalance suppressed? This research will help to design strategies to treat cancers holding inactivated Rb.

  Project II: Why do cancer cells need to express high level of FAS and how does FAS inhibition kill cancer cells? We will determine the role of FAS hyperactivity in cancer cells, and dissect the mechanism underlying FAS inhibition-induced cell death. Since targeting FAS has been reported to specifically kill cancer cells, many researchers from all over the world are trying to decipher the detailed mechanism but have failed to do so. It seems that it is not possible to explain FAS action in cancer cells by traditional cell signal transduction. We believe the answer will be found in select metabolic pathways that are critical for cancer cell homeostasis. This study is supposed to provide more targets either alone or together with FAS for the treatment of cancers.

  Project III: Irreversibly disrupting metabolic homeostasis specifically kills cancer cells. We will determine if metabolic pathways and constituent enzymes play essential roles in maintaining glucose, protein and lipid metabolic homeostasis, and whether they are potential therapeutic targets of cancer cells alone or in combination. We will then dissect the mechanisms by which disruption of metabolic homeostasis leads to cell death. We will set up a highthrough-put screening platform to identify the inhibitors of these pathways/enzymes.

  Project IV:Development of novel real-time measuring tools and new biotechnologies. We are trying to set up the research platforms for cancer metabolism and make real-time supervising tools/methods for the biological pathways.

  Selected Publications

  1、Tian W., Ma X., Zhang S., Sun Y. and Li B. Fatty Acid Synthase Inhibitors from Plants and Their Potential Application in the prevention of Metabolic Syndrome. Clin Oncol Cancer Res., 8: 1-9. (2011)

  2、Li B., Zhao J., Wang CZ, Searle J., He TC., Yuan CS., and Du W. Ginsenoside Rh2 induce apoptosis and paraptosis-like cell death in colon cancer cells through activation p53. Cancer Letters, 28;301(2):185-92. (2011)

  3、Li B., Gordon GM., Du CH., Xu J, and Du W. Specific killing of Rb mutant cancer cells by inactivating TSC2. Cancer Cell, 17: 469-480. (2010)

  Highlighted in Science(328: 1455, 2010)

  Comments in Cancer Research (70:5198, 2010)

  Evaluated in“F1000” by“Faculty Of 1000 Biology”.

  4、Li B., wang CZ., He TC., Yuan CS., and Du W. Antioxidants potentiate American ginseng-induced killing of colorectal cancer cells. Cancer Letters, 289 (1), 62-70. (2010).

  5、Li B., Zhang R., Sun YH., and Tian WX. Inactivation Mechanism of the β-Ketoacyl-[acyl carrier protein] Reductase of Bacterial Type II Fatty Acid Synthase by pigallocatechin Gallate. Biochem. Cell Biol., 84, 755-762 (2006).

  6、Li B., Ma XF., and Tian WX. Inhibitory Activity of Chlorogenic Acid on Enzymes Involved in the Fatty Acid Synthesis in Animals and Bacteria. IUBMB Life, 58, 39-46 (2006).

  7、Li B., Ma XF., Wang Y., Wang X., and Tian WX. Structure-Activity Relationships for Polyphenols Inhibiting Animal Fatty Acid Synthase. J. Biochem., 138, 679-686 (2005).

  8、Li B. and Tian WX. Inhibitory Effects of Flavonoids on Animal Fatty Acid Synthase. J. Biochem., 135, 85–91 (2004).

  9、Li B. and Tian WX. Presence of Fatty Acid Synthase Inhibitors in the Rhizome of Alpinia officinarum Hance. J. Enzyme Inhib. Med. Chem., 18, 349–356(2003).

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级PI  任秀宝

  任秀宝,主任医师,教授,博士生导师。1989年获临床学士学位,1996年获内科学硕士学位,同年到天津市肿瘤医院从事肿瘤生物治疗及内科综合治疗临床与基础研究工作至今。2006年获肿瘤学博士学位。于2001年赴日本TaKaRa研究所学习,于2006年到美国Vanderbilt大学肿瘤中心学习,2005年破格晋升为主任医师,2007年被评为博士生导师。现任天津医科大学肿瘤医院生物治疗科主任,生物技术研究室主任,天津市肿瘤免疫与生物治疗重点实验室主任。

  代表性文章:

  1. Shen M#, Wang J#, Yu W, Zhang C, Liu M, Wang K, Yang L, Wei F, Wang E*, Sun Q*, Ren X*. A novel MDSC-induced PD-1-PD-L1+ B-cell subset in breast tumor microenvironment possesses immuno-suppressive properties. OncoImmunology 2018 Feb 20;7(4):e1413520.

  2. Zhao H, Xu C, Luo X, Wei F, Wang N, Shi H, Ren X*. Seroprevalence of Neutralizing Antibodies against Human Adenovirus Type-5 and Chimpanzee Adenovirus Type-68 in Cancer Patients. Front Immunol. 2018 Mar 7;9:335.

  3. Sun Q, Li S, Wang Y, Peng H, Zhang X, Zheng Y, Li X, Li L, Chen R, Chen X, Bai W, Jiang X, Liu L, Wei F, Wang B, Zhang Y, Li H, Ren X*, Zhang H*. Phosphoglyceric acid mutase-1 contributes to oncogenic mTOR-mediated tumor growth and confers non-small cell lung cancer patients with poor prognosis. Cell Death and Differentiation, 2018 Jan 23.

  4. Li R, Li H, Sun Q, Liu L, Zhang C, Ren X*. Indoleamine 2,3-dioxygenase regulates T cell activity through Vav1/Rac pathway. Mol Immunol. 2017 Jan;81:102-107.

  5. Liu L, Zhang L, Yang L, Li H, Li R, Yu J, Yang L, Wei F, Yan C, Sun Q, Zhao H, Yang F, Jin H, Wang J, Wang SE, Ren X*. Anti-CD47 Antibody As a Targeted Therapeutic Agent for Human Lung Cancer and Cancer Stem Cells. Front Immunol. 2017 Apr 21;8:404.

  6. Wang K, Wang J, Wei F, Zhao N, Yang F, Ren X*. Expression of TLR4 in Non-Small Cell Lung Cancer Is Associated with PD-L1 and Poor Prognosis in Patients Receiving Pulmonectomy. Front Immunol. 2017 Apr 21;8:456.

  7. Wei F, Yang F, Li J, Zheng Y, Yu W, Yang L, Ren X*. Soluble Toll-like receptor 4 is a potential serum biomarker in non-small cell lung cancer. Oncotarget. 2016 Jun 28;7(26):40106-40114.

  8. Wang Y, Zhao H, Gao X, Wei F, Zhang X, Su Y, Wang C, Li H, Ren X*. Identification of a three-miRNA signature as a blood-borne diagnostic marker for early diagnosis of lung adenocarcinoma. Oncotarget. 2016 May 3;7(18):26070-86.

  9. Zhang L, Wang J, Wei F, Wang K, Sun Q, Yang F, Jin H, Zheng Y, Zhao H, Wang L, Yu W, Zhang X, An Y, Yang L, Zhang X, Ren X*. Profiling the dynamic expression of checkpoint molecules on cytokine-induced killer cells from non-small-cell lung cancer patients. 2016, Oncotarget. 2016 Jul 12;7(28):43604-43615.

  10. Zhao H, Wang Y, Yu J, Wei F, Cao S, Zhang X, Dong N, Li H, Ren X*. Autologous Cytokine-Induced Killer Cells Improves Overall Survival of Metastatic Colorectal Cancer Patients: Results From a Phase II Clinical Trial. Clin Colorectal Cancer.2016 Sep;15(3):228-35.

  11. Yan CH, Lv M, Li H, Song X, Yan F, Cao S, Ren X*. Osteopontin is a novel prognostic biomarker in early-stage non-small cell lung cancer after surgical resection. J Cancer Res Clin Oncol. 2015 Aug;141(8):1371-8.

  12. Hui Z, Zhang X, Ren B, Li R, Ren X*. Rapid Response of Advanced Squamous Non-Small Cell Lung Cancer with Thrombocytopenia after First-Line Treatment with Pembrolizumab Plus Autologous Cytokine-Induced Killer Cells. Front Immunol. 2015 Dec 17;6:633.

  13. Wei F, Yang F, Jiang X, Yu W, Ren X*. High-mobility group nucleosome-binding protein 1 is a novel clinical biomarker in non-small cell lung cancer. Tumour Biol. 2015 Dec;36(12):9405-10.

  14. Yu X, Zhao H, Liu L, Cao S, Ren B, Zhang N, An X, Yu J, Li H, Ren X*. A randomized phase II study of autologous cytokine-induced killer cells in treatment of hepatocellular carcinoma. J Clin Immunol 2014;34(2):194-203.

  15. Yu J, Wang Y, Yan F, Zhang P, Li H, Zhao H, Yan C, Yan F, Ren X*. Noncanonical NF-κB activation mediates STAT3-stimulated IDO upregulation in myeloid-derived suppressor cells in breast cancer. J Immunol. 2014 Sep 1;193(5):2574-86.

  16. Yu J, Du W, Yan F, Wang Y, Li H, Cao S, Yu W, Shen C, Liu J, Ren X*. Myeloid-derived suppressor cells suppress antitumor immune responses through IDO expression and correlate with lymph node metastasis in patients with breast cancer. J Immunol 2013;190(7):3783-97.

  17. Yang L, Ren B, Li H, Yu J, Cao S, Hao X, Ren X*. Enhanced antitumor effects of DC-activated CIKs to chemotherapy treatment in a single cohort of advanced non-small-cell lung cancer patients. Cancer Immunol Immunother 2013;62(1):65-73.

  18. Liu L, Zhang W, Qi X, Li H, Yu J, Wei S, Hao X, Ren X*. Randomized study of autologous cytokine-induced killer cell immunotherapy in metastatic renal carcinoma. Clin Cancer Res 2012;18(6):1751-9.

  著作:

  主编《实体肿瘤细胞免疫治疗》,2010年出版第一版,2015年应人民卫生出版社要求出版第二版,总印数12000册。参编《腹部肿瘤学》、《简明肿瘤学》、《头颈部肿瘤学》、《肿瘤学新进展》等多部肿瘤学专著。

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级PI  张宁

  张宁,男,教授,973首席科学家、国家“万人计划”入选者、国家杰出青年科学基金获得者、科技部中青年科技创新领军人才、国家“百千万人才”工程入选者、天津市杰出人才、教育部新世纪优秀人才、天津市特聘教授、天津市“千人计划”入选者。现担任北京大学医学部副主任,天津医科大学肿瘤医院研究所PI,中国抗癌协会常务理事、副秘书长,《Cancer Biology & Medicine》常务副主编。

  张宁教授长期从事生物医学及细胞生物学研究,围绕癌转移这一关键临床难题,从机理研究、生物标志物鉴定、药物筛选、分子遗传学、纳米技术等多个侧面入手展开转化应用研究,取得了一系列科研成果。发现并阐述了PKCζ、PDK1、Akt2、Rictor、ELMO1、Txnl2等一系列信号分子调控细胞运动的功能和机理,初步揭示了一个调控癌细胞趋化运动的信号传导通路。建立了一个新的药物筛选细胞模型,筛选获得两个先导化合物,一个抗癌转移化合物,已申请专利并开展临床前研究工作。在纳米肿瘤学领域,进行纳米技术在肿瘤诊疗中的应用研究,建立了一系列肿瘤纳米检测新方法和手段,构建了一系列纳米新材料。在肿瘤遗传学研究方面,揭示了肝细胞肝癌不同病灶间的基因组图谱及其克隆进化关系,为肝癌的诊疗、预后判断以及微转移机理研究提供了依据。结合单细胞捕获及单细胞基因组技术,证明了CTC拷贝数变化具有癌种特异性,并揭示了原位肿瘤细胞中拷贝数变化连续的进化过程,该研究是世界上首次大规模的多癌种CTC单细胞全基因组检测。

  基于以上研究,张宁教授近五年在Gastroenterology、Genome Research、Nature Communications、Biomaterials、Cancer Research、Nano Research、Molecular & Cellular Proteomics等国际期刊中发表SCI文章52篇,总IF为310.725,其中36篇为通讯作者或共同通讯作者,IF为224.109;获得授权专利2项;作为项目负责人,主持了包括国家重大科学研究计划项目、863计划课题,国家杰出青年科学基金、国家自然基金中加合作项目、面上项目等在内的多项国家级及省部级课题。

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稿源:天津市肿瘤医院                                        编辑:科教处
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