000130298 001__ 130298
000130298 005__ 20240228143423.0
000130298 0247_ $$2doi$$a10.1016/j.ccell.2016.10.018
000130298 0247_ $$2pmid$$apmid:27960088
000130298 0247_ $$2ISSN$$a1535-6108
000130298 0247_ $$2ISSN$$a1878-3686
000130298 0247_ $$2altmetric$$aaltmetric:14681074
000130298 037__ $$aDKFZ-2017-05377
000130298 041__ $$aeng
000130298 082__ $$a610
000130298 1001_ $$aPark, Jin-Sung$$b0
000130298 245__ $$aNormalization of Tumor Vessels by Tie2 Activation and Ang2 Inhibition Enhances Drug Delivery and Produces a Favorable Tumor Microenvironment.
000130298 260__ $$aCambridge, Mass.$$bCell Press$$c2016
000130298 3367_ $$2DRIVER$$aarticle
000130298 3367_ $$2DataCite$$aOutput Types/Journal article
000130298 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1521187219_1713
000130298 3367_ $$2BibTeX$$aARTICLE
000130298 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000130298 3367_ $$00$$2EndNote$$aJournal Article
000130298 520__ $$aA destabilized tumor vasculature leads to limited drug delivery, hypoxia, detrimental tumor microenvironment, and even metastasis. We performed a side-by-side comparison of ABTAA (Ang2-Binding and Tie2-Activating Antibody) and ABA (Ang2-Blocking Antibody) in mice with orthotopically implanted glioma, with subcutaneously implanted Lewis lung carcinoma, and with spontaneous mammary cancer. We found that Tie2 activation induced tumor vascular normalization, leading to enhanced blood perfusion and chemotherapeutic drug delivery, markedly lessened lactate acidosis, and reduced tumor growth and metastasis. Moreover, ABTAA favorably altered the immune cell profile within tumors. Together, our findings establish that simultaneous Tie2 activation and Ang2 inhibition form a powerful therapeutic strategy to elicit a favorable tumor microenvironment and enhanced delivery of a chemotherapeutic agent into tumors.
000130298 536__ $$0G:(DE-HGF)POF3-311$$a311 - Signalling pathways, cell and tumor biology (POF3-311)$$cPOF3-311$$fPOF III$$x0
000130298 588__ $$aDataset connected to CrossRef, PubMed,
000130298 650_7 $$2NLM Chemicals$$aAntibodies
000130298 650_7 $$2NLM Chemicals$$aAntineoplastic Agents
000130298 650_7 $$07GR28W0FJI$$2NLM Chemicals$$aDacarbazine
000130298 650_7 $$0EC 2.7.10.1$$2NLM Chemicals$$aReceptor, TIE-2
000130298 650_7 $$0EC 2.7.10.1$$2NLM Chemicals$$aTek protein, mouse
000130298 650_7 $$0EC 3.1.27.5$$2NLM Chemicals$$aAng2 protein, mouse
000130298 650_7 $$0EC 3.1.27.5$$2NLM Chemicals$$aRibonuclease, Pancreatic
000130298 650_7 $$0YF1K15M17Y$$2NLM Chemicals$$atemozolomide
000130298 7001_ $$aKim, Il-Kug$$b1
000130298 7001_ $$aHan, Sangyeul$$b2
000130298 7001_ $$aPark, Intae$$b3
000130298 7001_ $$aKim, Chan$$b4
000130298 7001_ $$aBae, Jeomil$$b5
000130298 7001_ $$aOh, Seung Ja$$b6
000130298 7001_ $$aLee, Seungjoo$$b7
000130298 7001_ $$aKim, Jeong Hoon$$b8
000130298 7001_ $$aWoo, Dong-Cheol$$b9
000130298 7001_ $$aHe, Yulong$$b10
000130298 7001_ $$0P:(DE-He78)2e92d0ae281932fc7347d819fec36b0b$$aAugustin, Hellmut$$b11$$udkfz
000130298 7001_ $$aKim, Injune$$b12
000130298 7001_ $$aLee, Doheon$$b13
000130298 7001_ $$aKoh, Gou Young$$b14
000130298 773__ $$0PERI:(DE-600)2074034-7$$a10.1016/j.ccell.2016.10.018$$gVol. 30, no. 6, p. 953 - 967$$n6$$p953 - 967$$tCancer cell$$v30$$x1535-6108$$y2016
000130298 909CO $$ooai:inrepo02.dkfz.de:130298$$pVDB
000130298 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)2e92d0ae281932fc7347d819fec36b0b$$aDeutsches Krebsforschungszentrum$$b11$$kDKFZ
000130298 9131_ $$0G:(DE-HGF)POF3-311$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vSignalling pathways, cell and tumor biology$$x0
000130298 9141_ $$y2016
000130298 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bCANCER CELL : 2015
000130298 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000130298 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000130298 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000130298 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search
000130298 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC
000130298 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000130298 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000130298 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000130298 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000130298 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine
000130298 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000130298 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000130298 915__ $$0StatID:(DE-HGF)9920$$2StatID$$aIF >= 20$$bCANCER CELL : 2015
000130298 9201_ $$0I:(DE-He78)A190-20160331$$kA190$$lVaskuläre Onkologie und Metastasierung$$x0
000130298 980__ $$ajournal
000130298 980__ $$aVDB
000130298 980__ $$aI:(DE-He78)A190-20160331
000130298 980__ $$aUNRESTRICTED