001     130298
005     20240228143423.0
024 7 _ |a 10.1016/j.ccell.2016.10.018
|2 doi
024 7 _ |a pmid:27960088
|2 pmid
024 7 _ |a 1535-6108
|2 ISSN
024 7 _ |a 1878-3686
|2 ISSN
024 7 _ |a altmetric:14681074
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037 _ _ |a DKFZ-2017-05377
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Park, Jin-Sung
|b 0
245 _ _ |a Normalization of Tumor Vessels by Tie2 Activation and Ang2 Inhibition Enhances Drug Delivery and Produces a Favorable Tumor Microenvironment.
260 _ _ |a Cambridge, Mass.
|c 2016
|b Cell Press
336 7 _ |a article
|2 DRIVER
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336 7 _ |a Journal Article
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|s 1521187219_1713
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a A 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.
536 _ _ |a 311 - Signalling pathways, cell and tumor biology (POF3-311)
|0 G:(DE-HGF)POF3-311
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588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Antibodies
|2 NLM Chemicals
650 _ 7 |a Antineoplastic Agents
|2 NLM Chemicals
650 _ 7 |a Dacarbazine
|0 7GR28W0FJI
|2 NLM Chemicals
650 _ 7 |a Receptor, TIE-2
|0 EC 2.7.10.1
|2 NLM Chemicals
650 _ 7 |a Tek protein, mouse
|0 EC 2.7.10.1
|2 NLM Chemicals
650 _ 7 |a Ang2 protein, mouse
|0 EC 3.1.27.5
|2 NLM Chemicals
650 _ 7 |a Ribonuclease, Pancreatic
|0 EC 3.1.27.5
|2 NLM Chemicals
650 _ 7 |a temozolomide
|0 YF1K15M17Y
|2 NLM Chemicals
700 1 _ |a Kim, Il-Kug
|b 1
700 1 _ |a Han, Sangyeul
|b 2
700 1 _ |a Park, Intae
|b 3
700 1 _ |a Kim, Chan
|b 4
700 1 _ |a Bae, Jeomil
|b 5
700 1 _ |a Oh, Seung Ja
|b 6
700 1 _ |a Lee, Seungjoo
|b 7
700 1 _ |a Kim, Jeong Hoon
|b 8
700 1 _ |a Woo, Dong-Cheol
|b 9
700 1 _ |a He, Yulong
|b 10
700 1 _ |a Augustin, Hellmut
|0 P:(DE-He78)2e92d0ae281932fc7347d819fec36b0b
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|u dkfz
700 1 _ |a Kim, Injune
|b 12
700 1 _ |a Lee, Doheon
|b 13
700 1 _ |a Koh, Gou Young
|b 14
773 _ _ |a 10.1016/j.ccell.2016.10.018
|g Vol. 30, no. 6, p. 953 - 967
|0 PERI:(DE-600)2074034-7
|n 6
|p 953 - 967
|t Cancer cell
|v 30
|y 2016
|x 1535-6108
909 C O |o oai:inrepo02.dkfz.de:130298
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910 1 _ |a Deutsches Krebsforschungszentrum
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|b 11
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|l Krebsforschung
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914 1 _ |y 2016
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