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| 1 | 巨噬细胞的免疫重塑:防治肿瘤转移的新靶点显示文摘动态变化的炎性环境是肿瘤不断恶变并发生转移的重要原因。巨噬细胞作为肿瘤间质中主要的炎症细胞,在肿瘤微环境的刺激下,发生了表型和功能的改变,促进肿瘤的恶性进展。因此,研发选择性的调控巨噬细胞免疫重塑的药物,可能成为肿瘤靶向治疗的新策略。但是,肿瘤微环境中调控巨噬细胞表型转化的关键事件及分子网络目前尚未明确。我们的研究发现,先天性免疫机制中重要的衔接蛋白CARD9(caspase recruitment domain-containing protein 9),通过促进骨髓来源的巨噬细胞向转移相关的表型分化,进而在结肠癌肝转移中起关键作用。组织蛋白酶Cat S(cathepsin S)通过介导巨噬细胞自噬过程,促进巨噬细胞向M2型分化,加重肿瘤转移。相反,结肠癌中黏附分子1(ICAM-1)通过调控巨噬细胞的吞噬功能,抑制肿瘤相关巨噬细胞向M2型分化,阻滞肿瘤转移。我们新近的研究发现,在转移微环境中M2型巨噬细胞促进肿瘤细胞由上皮型向间质型转化,加重转移灶形成;相反,M1型巨噬细胞导致肿瘤细胞由间质型向上皮型转分化,导致转移灶中存活的肿瘤细胞处于休眠状态。综上,我们以肿瘤微环境中巨噬细胞的分化、自噬、吞噬及调控肿瘤细胞表型为切入点,以期发现调节肿瘤转移的分子靶点,为肿瘤免疫治疗提供更多的依据,并且提供新的防治肿瘤转移的药物靶点。 | 杨敏 杜杰 Alan WELLS | 2016 | 中国药理学与毒理学杂志2016，30，10： | 3 |
| 2 | Gold modified cobalt-based Fischer-Tropsch catalysts for conversion of synthesis gas to liquid fuels显示文摘 | Alan J. Mccue Jura Aponaviciute Richard P.K. Wells James A. Anderson | 2013 | Frontiers of Chemical Science and Engineering2013，7，3： | 1 |
| 3 | Mathematical modeling of epidermal growth factor receptor signaling through the phospholipse C pathway: Mechanistic insights and predictions for molecular interventions显示文摘 | Alan Wells Lauffenburger DA | 2000 | Biotechnol Bioeng2000，70，10： | 1 |
| 4 | Dispute Resolution : Mediation and Arbitration 显示文摘 | Alan Wells | 2011 | Business Law Review2011，，32： | 1 |
| 5 | Atrial Tachycardia After Circumferential Pulmonary Vein Ablation of Atrial Fibrillation显示文摘 | Sanders Chae Hakan Oral Eric Good Sujoya Dey Alan Wimmer Thomas Crawford Darryl Wells Jean-Francois Sarrazin Nagib Chalfoun Michael Kuhne Jackie Fortino Elizabeth Huether Tammy Lemerand Frank Pelosi Frank Bogun Fred Morady Aman Chugh | 2007 | Journal of the American College of Cardiology2007，，18： | 1 |
| 6 | 1-[3-Aminobenzisoxazol-5′-yl]-3-trifluoromethyl-6-[2′-(3-( R )-hydroxy- N -pyrrolidinyl)methyl-[1,1′]-biphen-4-yl]-1,4,5,6-tetrahydropyrazolo-[3,4- c ]-pyridin-7-one (BMS-740808) a highly potent, selective, efficacious, and orally bioavailable inhibitor o显示文摘 | Donald J.P. Pinto Michael J. Orwat Mimi L. Quan Qi Han Robert A. Galemmo Eugene Amparo Brian Wells Christopher Ellis Ming Y. He Richard S. Alexander Karen A. Rossi Angela Smallwood Pancras C. Wong Joseph M. Luettgen Alan R. Rendina Robert M. Knabb Lawrenc | 2006 | Bioorganic & Medicinal Chemistry Letters2006，，15： | 1 |
| 7 | Molecules in focus EGF receptor 显示文摘 | ALAN wells | 1999 | The Internation- al Journal of Biochemistry & Cell Biology1999，31，： | 1 |
| 8 | Fatty Acid -Induced Insulin Resistance in Adipocytes显示文摘 | MARK VAN EPPS-FUNG JODIE WILLIFORD ALAN WELLS | 1997 | Endocrinology1997，138，10： | 1 |
| 9 | Transcriptional suppression of Matrix Metalloproteinase-2 gene expression in human ostrraglioma cells by TNF-α and TNF-γ显示文摘 | Jason D Moellinger Alan wells | 1998 | J Immunol1998，161，： | 1 |
| 10 | Potent antitumor activity of cabozantinib, a c‐ MET and VEGFR 2 inhibitor, in a colorectal cancer patient‐derived tumor explant model显示文摘 | Eun‐Kee Song WM Tai Wells A. Messersmith Stacey Bagby Alicia Purkey Kevin S. Quackenbush Todd M. Pitts Guoliang Wang Patrick Blatchford Rachel Yahn Jeffrey Kaplan Aik Choon Tan Chloe E. Atreya Gail Eckhardt Robin K. Kelley Alan Venook Eunice L. Kwak David | 2015 | Int. J. Cancer2015，，8： | 1 |
| 11 | EGF receptor显示文摘 | Alan Wells | 1999 | International Journal of Biochemistry and Cell Biology1999，，6： | 1 |
| 12 | Innate Immune Interleukin-1 Receptor–Associated Kinase 4 Exacerbates Viral Myocarditis by Reducing CCR5+CD11b+ Monocyte Migration and Impairing Interferon Production显示文摘 | Alan Valaperti Mototsugu Nishii Youan Liu Kotaro Naito Megan Chan Liyong Zhang Carsten Skurk Heinz-Peter Schultheiss George A. Wells Urs Eriksson Peter P. Liu | 2013 | Circulation2013，，14： | 1 |
| 13 | Association of abnormal morphology and altered gene expression in human preimplantation embryos显示文摘 | Dagan Wells Mercedes G. Bermúdez Nury Steuerwald Henry E. Malter Alan R. Thornhill Jacques Cohen | 2005 | Fertility and Sterility2005，，2： | 1 |
| 14 | Combining Static Worst-case Execution Time Analysis and Program Proof显示文摘 | Roderick Chapman Alan Burns Andy Wellings | | Real-Time Systems 110，，： | 1 |
| 15 | E-cadherin as an indicator of mesenchymal to epithelial reverting transitions during the metastatic seeding of disseminated carcinomas显示文摘 | Alan Wells Clayton Yates Christopher R. Shepard | 2008 | Clinical & Experimental Metastasis2008，，6： | 1 |
| 16 | Phospholipase C-γ1 in tumor progression显示文摘 | Alan Wells Jennifer Rubin Grandis | 2003 | Clinical and Experimental Metastasis2003，，4： | 1 |
| 17 | Molecules in focus EGF receptor 显示文摘 | Alan Wells | 1999 | Int J Biochem Cell Biol1999，31，： | 1 |
| 18 | Nuclear Kaiso Indicates Aggressive Prostate Cancers and Promotes Migration and Invasiveness of Prostate Cancer Cells显示文摘 | Jacqueline Jones Honghe Wang Jianjun Zhou Shana Hardy Timothy Turner David Austin Qinghua He Alan Wells William E. Grizzle Clayton Yates | 2012 | The American Journal of Pathology2012，，5： | 1 |
| 19 | Akt isoforms differentially provide for chemoresistance in prostate cancer显示文摘Objective:Early prostate cancer micrometastatic foci undergo a mesenchymal to epithelial reverting transition,not only aiding seeding and colonization,but also rendering the tumor cells generally chemoresistant.We previously found that upregulated E-cadherin in the epithelial micrometastases activated canonical survival pathways,including PI3K-Akt,that protected the tumor cells from death;however,the extent of protection from blocking the pathway in its entirety was modest,because different isoforms may have alternately affected cell functioning.Here,we characterized Akt isoform expressions in primary and metastatic prostate cancers,as well as their individual contributions to chemoresistance.Methods:Akt isoforms and E-cadherin were manipulated with drugs,knocked down,and over expressed.Tumor cell killing was determined in vitro and in vivo.Overall survival was calculated from patient records and specimens.Results:Pan-Akt inhibition sensitized tumor cells to chemotherapy,and specific blockade of Akt1 or/and Akt2 caused cells to be more chemoresponsive.Overexpression of Akt3 induced apoptosis.A low dose of Akt1 or Akt2 inhibitor enabled standard chemotherapies to significantly eradicate metastatic prostate tumors in a mouse model,acting as chemosensitizers.In human specimens,we found Akt1 and Akt2 positively correlated,whereas Akt3 inversely correlated,with the overall survival of prostate cancer patients.Akt1high/Akt2high/Akt3low tumors had the worst outcomes.Conclusions:E-cadherin-induced activation of Akt1/2 isoforms was the essential mechanism of chemoresistance,whereas Akt3 made cells more fragile.These findings emphasized the need to target Akt1/2,rather than pan-Akt,as a rational therapeutic approach. | Bo Ma Hanshuang Shao Xia Jiang Zhou Wang Chuanyue(Cary)Wu Diana Whaley Alan Wells | 2022 | Cancer Biology & Medicine2022，19，5： | 0 |
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