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Antiangiogenic Therapy Induces Hepatic Tumor Vascular Network Rearrangement to Receive Perfusion via the Portal Vein and Hepatic Artery
DC Field | Value | Language |
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dc.contributor.author | 김한솔 | - |
dc.contributor.author | 박미숙 | - |
dc.contributor.author | 임준석 | - |
dc.date.accessioned | 2017-10-26T07:33:10Z | - |
dc.date.available | 2017-10-26T07:33:10Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 1018-1172 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/152182 | - |
dc.description.abstract | PURPOSE: Hepatic malignancies can easily develop resistance to antiangiogenic therapy, but the underlying mechanism remains poorly understood. This study explores whether antiangiogenic therapy influences the tumor vascular network and/or the vessels feeding the hepatic tumor. METHODS: Mice implanted with Lewis lung carcinoma (LLC) cells were subcutaneously injected 3 times (once every other day starting 1 week after LLC implantation) with either an antiangiogenic agent [vascular endothelial growth factor (VEGF)-Trap] or control agent (bovine serum albumin) at a dose of 25 mg/kg before performing angiography. Hepatic arteriography and portography were performed using a vascular cast method with vascular latex. RESULTS: Arteriography of the control-treated LLC-implanted mice showed marked staining of the mass with a prominent feeding artery, suggesting that the tumor is supplied by arterial perfusion. No significant staining was observed on portography. By contrast, 33% (n = 3/9) of the LLC-implanted mice treated with the antiangiogenic agent VEGF-Trap showed intratumoral staining during portography, indicating that these tumors received perfusion via the portal vein. CONCLUSION: Antiangiogenic treatment can induce rearrangement of the hepatic tumor vascular network to establish communication with the portal vein. This implies that hepatic tumors can develop resistance to antiangiogenic therapy by maintaining perfusion through portal venous perfusion. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | S. Karger | - |
dc.relation.isPartOf | JOURNAL OF VASCULAR RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Angiogenesis Inhibitors/administration & dosage* | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Carcinoma, Lewis Lung/blood supply | - |
dc.subject.MESH | Carcinoma, Lewis Lung/diagnostic imaging | - |
dc.subject.MESH | Carcinoma, Lewis Lung/drug therapy* | - |
dc.subject.MESH | Carcinoma, Lewis Lung/pathology | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Drug Resistance, Neoplasm* | - |
dc.subject.MESH | Hepatic Artery*/diagnostic imaging | - |
dc.subject.MESH | Infusions, Intra-Arterial | - |
dc.subject.MESH | Infusions, Intravenous | - |
dc.subject.MESH | Liver Neoplasms, Experimental/blood supply | - |
dc.subject.MESH | Liver Neoplasms, Experimental/diagnostic imaging | - |
dc.subject.MESH | Liver Neoplasms, Experimental/drug therapy* | - |
dc.subject.MESH | Liver Neoplasms, Experimental/pathology | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Mice, Inbred C57BL | - |
dc.subject.MESH | Neovascularization, Pathologic* | - |
dc.subject.MESH | Portal Vein*/diagnostic imaging | - |
dc.subject.MESH | Receptors, Vascular Endothelial Growth Factor/administration & dosage* | - |
dc.subject.MESH | Recombinant Fusion Proteins/administration & dosage* | - |
dc.subject.MESH | Time Factors | - |
dc.title | Antiangiogenic Therapy Induces Hepatic Tumor Vascular Network Rearrangement to Receive Perfusion via the Portal Vein and Hepatic Artery | - |
dc.type | Article | - |
dc.publisher.location | Switzerland | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Radiology | - |
dc.contributor.googleauthor | Kang W. | - |
dc.contributor.googleauthor | Lim J.S. | - |
dc.contributor.googleauthor | Park M. | - |
dc.contributor.googleauthor | Koh G.Y. | - |
dc.contributor.googleauthor | Kim H. | - |
dc.identifier.doi | 10.1159/000448734 | - |
dc.contributor.localId | A01463 | - |
dc.contributor.localId | A03408 | - |
dc.contributor.localId | A01099 | - |
dc.relation.journalcode | J01923 | - |
dc.identifier.eissn | 1423-0135 | - |
dc.identifier.pmid | 27643516 | - |
dc.identifier.url | https://www.karger.com/Article/Abstract/448734 | - |
dc.contributor.alternativeName | Kim, Hon Soul | - |
dc.contributor.alternativeName | Park, Mi Sook | - |
dc.contributor.alternativeName | Lim, Joon Seok | - |
dc.contributor.affiliatedAuthor | Park, Mi-Suk | - |
dc.contributor.affiliatedAuthor | Lim, Joon Seok | - |
dc.contributor.affiliatedAuthor | Kim, Hon Soul | - |
dc.citation.volume | 53 | - |
dc.citation.number | 1~2 | - |
dc.citation.startPage | 72 | - |
dc.citation.endPage | 82 | - |
dc.identifier.bibliographicCitation | JOURNAL OF VASCULAR RESEARCH, Vol.53(1~2) : 72-82, 2016 | - |
dc.date.modified | 2017-10-24 | - |
dc.identifier.rimsid | 46960 | - |
dc.type.rims | ART | - |
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