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陳可欣，博士，教授，博士生導師,，現(xiàn)任天津醫(yī)科大學腫瘤醫(yī)院副院長，教育部創(chuàng)新團隊發(fā)展計劃及滾動支持帶頭人,，國家衛(wèi)生計生突出貢獻中青年專家,，天津市“十一五”“十二五”綜合投資重點學科帶頭人,，曾榮獲天津市“五一勞動獎?wù)?span style="color: rgb(0, 0, 0); font-family: 宋體, Arial, Helvetica, sans-serif; text-align: justify;">”和“天津市優(yōu)秀回國人員”稱號。中國抗癌協(xié)會腫瘤流行病學專業(yè)會員會副主任委員,，天津市預(yù)防醫(yī)學會流行病分會主任委員,，天津市吸煙與健康協(xié)會理事會副會長，天津醫(yī)學會臨床流行病學專業(yè)委會常委,，國際腫瘤登記報告協(xié)會(IACR)的會員,、中國腫瘤登記報告協(xié)會的常務(wù)理事；現(xiàn)為《Cancer Medicine》,、《Chinese Journal of Cancer》,、《中國腫瘤臨床》等雜志編委。
1987年畢業(yè)于天津醫(yī)科大學,，獲公共衛(wèi)生學士學位,。同年分配到天津市腫瘤醫(yī)院流行病學研究室，從事腫瘤流行病學研究工作,。2003年獲碩士學位,，2007年獲博士學位。
長期從事腫瘤流行病學研究工作,，包括天津惡性腫瘤的流行趨勢研究,、常見惡性腫瘤的早期篩查和腫瘤分子流行病學的研究。作為腫瘤重點研究方向之一,，與所在單位一起成功申請腫瘤國家重點學科,、乳腺癌防治教育部重點實驗室和創(chuàng)新團隊。2006年作為學科帶頭人獲得天津市“十一五”,、“十二五”綜合投資重點學科,，2010年獲得中央財政支持地方高校發(fā)展專項資金腫瘤流行病重點學科，2011年獲得教育部“常見惡性腫瘤預(yù)防的研究”創(chuàng)新團隊,，并于2015年獲教育部創(chuàng)新團隊滾動支持,。
作為項目負責人主持教育部創(chuàng)新團隊發(fā)展計劃基金及滾動支持項目、國家自然科學基金重大國際(地區(qū))合作與交流項目1項,、863專項1項,、科技部新藥創(chuàng)制平臺項目1項、國家自然科學基金3項,、省部級基金項目8項,、NCI、UICC等國際合作項目10余項,。獲得9項省部級以上科技進步獎,，其中作為第二完成人獲得國家科技進步二等獎和天津市科技進步一等獎各一項，作為第一完成人獲得天津市科技進步一等獎,、三等獎和中國抗癌協(xié)會科技一等獎各一項,。近5年發(fā)表學術(shù)論文近百篇，其中SCI論文76篇,，影響因子IF>10論文15篇,，他引頻次1038次，其中第一/通訊作者文章35篇,，單篇最高引用頻次165次,，研究成果發(fā)表在Annals of Oncology、 Nature Communications,、Hepatology,、Cancer Cell、Nature Genetics,、J Clinical Invest,、PNAS、International Journal of Epidemiology,、Clinical Cancer Res,、 Carcinogenesis等專業(yè)研究的雜志。
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馮玉梅,，女,，1965年1月出生，博士,，研究員,，教授，博士生導師,，天津市“131”創(chuàng)新型人才第一層次人選,。1983-1987年大學本科就讀于于南開大學化學系應(yīng)用化學專業(yè)，1987-1990年碩士研究生就讀于南開大學分子生物學研究所生物化學專業(yè),，自1990年畢業(yè)至今在天津醫(yī)科大學腫瘤醫(yī)院腫瘤研究所工作,，2003年晉升為研究員，2006年兼聘為教授,，2007年遴選為博士研究生導師,。自2000年至今任生物化學與分子生物學研究室主任，兼任中國抗癌協(xié)會腫瘤標志專業(yè)委員會委員(第二,、三,、四、五屆),，中國抗癌協(xié)會乳腺癌專業(yè)委員會委員(第四,、五屆)，天津市細胞生物學會理事(第一,、二屆),，《中國腫瘤臨床》雜志編委(第四屆),。2006-2009年于天津大學在職攻讀博士學位。研究方向為腫瘤分子生物學,，致力于乳腺癌轉(zhuǎn)移機制研究和腫瘤基因診斷研究,。主持國家自然科學基金面上項目5項、天津市自然科學基金重點項目2項,、國家“九五”科技攻項目關(guān)子課題,、國家“863”計劃子課題、國家科技支撐計劃子課題等,；作為第一完成人獲天津市自然科學三等獎,、天津市科技進步三等獎、天津市衛(wèi)生局科技成果一等獎,、天津醫(yī)科大學科技成果二等獎各1項,；作為通訊作者發(fā)表SCI論文20篇，至今他引415次,，其中一篇入選全球Top 1% ESI高被引優(yōu)秀論文,；指導博士研究生12名、碩士研究生32名,，其中3人獲天津醫(yī)科大學優(yōu)秀博碩士畢業(yè)生,、1人獲天津醫(yī)科大學優(yōu)秀博士論文獎勵。
代表性論文(*為通訊作者)
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.
聯(lián)系電話：022-23340123轉(zhuǎn)6002
E-mail：[email protected], [email protected]
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李兵輝,，博士,，教授，PI,，博士生導師
教育背景
2001.09~2006.04理學博士,，中國科學院研究生院。專業(yè)：生物化學與分子生物學,。
1996.09~2000.07理學學士,，江西南昌大學。專業(yè)：生物工程,。
工作經(jīng)歷
2007.11~2010.10研究助理(Research Professional Associate),，芝加哥大學。從事癌癥與能量代謝方面的研究,。
2010.12~至今教授,，天津醫(yī)科大學附屬腫瘤醫(yī)院腫瘤研究所。
研究興趣
本課題組將著重闡述代謝酶,、代謝產(chǎn)物及癌細胞命運之間的關(guān)系,，以尋找新穎的、特異的抗癌靶點為主要任務(wù)！我們的研究興趣在：
1,、腫瘤生長抑制因子Rb通過控制能量代謝平衡調(diào)節(jié)細胞轉(zhuǎn)化作用的機制研究,。本課題組擬解決Rb是如何控制代謝平衡的及Rb失活的癌細胞是如何控制代謝失衡的，并從中找出能特異殺死Rb失活的癌細胞的分子靶點,，為癌癥治療帶來新方法,、新理念！
2,、研究和代謝相關(guān)的脂肪酸合成,、蛋白質(zhì)合成紊亂(ER Stress)及自噬(Autophagy)發(fā)生的機制及它們和腫瘤發(fā)生發(fā)展的關(guān)系,。
3,、能量代謝如何決定細胞的命運。近些年來,，科學家們逐漸意識到幾乎所有的細胞信號轉(zhuǎn)導途徑最終都匯集在代謝網(wǎng)絡(luò)上,，這迅速催熱了癌癥的代謝研究。細胞的代謝是如何決定細胞命運的,？是如何決定細胞的轉(zhuǎn)化的,？我們的研究將著重理清癌細胞中糖代謝、脂代謝及蛋白質(zhì)代謝之間的關(guān)系,，尋找癌細胞得以轉(zhuǎn)化的物質(zhì)基礎(chǔ)(代謝本質(zhì)),。
4、開發(fā)實時生物學功能監(jiān)測工具,。我們將致力于確定研究細胞代謝(決定細胞命運)的方法,；將致力于開發(fā)實時監(jiān)測代謝平衡及細胞凋亡的工具。
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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任秀寶,，主任醫(yī)師,，教授，博士生導師,。1989年獲臨床學士學位,，1996年獲內(nèi)科學碩士學位，同年到天津市腫瘤醫(yī)院從事腫瘤生物治療及內(nèi)科綜合治療臨床與基礎(chǔ)研究工作至今。2006年獲腫瘤學博士學位,。于2001年赴日本TaKaRa研究所學習,，2005年破格晉升為主任醫(yī)師，2007年被評為博士生導師�,，F(xiàn)任天津醫(yī)科大學腫瘤醫(yī)院生物治療科主任,，生物技術(shù)研究室主任，天津市腫瘤免疫與生物治療重點實驗室主任,。
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：
主編《實體腫瘤細胞免疫治療》,，2010年出版第一版，2015年應(yīng)人民衛(wèi)生出版社要求出版第二版,，總印數(shù)12000冊,。參編《腹部腫瘤學》、《簡明腫瘤學》,、《頭頸部腫瘤學》,、《腫瘤學新進展》等多部腫瘤學專著。
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張寧,，男,，教授，973首席科學家,、國家“萬人計劃”入選者,、國家杰出青年科學基金獲得者、科技部中青年科技創(chuàng)新領(lǐng)軍人才,、國家“百千萬人才”工程入選者,、天津市杰出人才、教育部新世紀優(yōu)秀人才�,，F(xiàn)擔任北京大學醫(yī)學部副主任,，天津醫(yī)科大學腫瘤醫(yī)院研究所PI，中國抗癌協(xié)會常務(wù)理事,、副秘書長,，《Cancer Biology & Medicine》常務(wù)副主編。
張寧教授長期從事生物醫(yī)學及細胞生物學研究,，圍繞癌轉(zhuǎn)移這一關(guān)鍵臨床難題,，從機理研究、生物標志物鑒定,、藥物篩選,、分子遺傳學、納米技術(shù)等多個側(cè)面入手展開轉(zhuǎn)化應(yīng)用研究,，取得了一系列科研成果,。發(fā)現(xiàn)并闡述了PKCζ、PDK1、Akt2,、Rictor,、ELMO1、Txnl2等一系列信號分子調(diào)控細胞運動的功能和機理,，初步揭示了一個調(diào)控癌細胞趨化運動的信號傳導通路,。建立了一個新的藥物篩選細胞模型，篩選獲得兩個先導化合物,，一個抗癌轉(zhuǎn)移化合物,，已申請專利并開展臨床前研究工作。在納米腫瘤學領(lǐng)域,，進行納米技術(shù)在腫瘤診療中的應(yīng)用研究,，建立了一系列腫瘤納米檢測新方法和手段，構(gòu)建了一系列納米新材料,。在腫瘤遺傳學研究方面,，揭示了肝細胞肝癌不同病灶間的基因組圖譜及其克隆進化關(guān)系,，為肝癌的診療,、預(yù)后判斷以及微轉(zhuǎn)移機理研究提供了依據(jù)。結(jié)合單細胞捕獲及單細胞基因組技術(shù),，證明了CTC拷貝數(shù)變化具有癌種特異性,，并揭示了原位腫瘤細胞中拷貝數(shù)變化連續(xù)的進化過程，該研究是世界上首次大規(guī)模的多癌種CTC單細胞全基因組檢測,。
基于以上研究,，張寧教授近五年在Gastroenterology、Genome Research,、Nature Communications,、Biomaterials、Cancer Research,、Nano Research,、Molecular & Cellular Proteomics等國際期刊中發(fā)表SCI文章52篇，總IF為310.725,，其中36篇為通訊作者或共同通訊作者,，IF為224.109；獲得授權(quán)專利2項,；作為項目負責人,，主持了包括國家重大科學研究計劃項目、863計劃課題,，國家杰出青年科學基金,、國家自然基金中加合作項目、面上項目等在內(nèi)的多項國家級及省部級課題。
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