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Please use this identifier to cite or link to this item: http://hdl.handle.net/10564/2322

Title: Synergistic inhibitory effect of gemcitabine and angiotensin type-1 receptor blocker, losartan, on murine pancreatic tumor growth via anti-angiogenic activities.
Authors: Noguchi, Ryuichi
Yoshiji, Hitoshi
Ikenaka, Yasuhide
Namisaki, Tadashi
Kitade, Mitsuteru
Kaji, Kosuke
Yoshii, Junichi
Yanase, Koji
Yamazaki, Masaharu
Tsujimoto, Tatsuhiro
Kawaratani, Hideto
Fukui, Hiroshi
Keywords: VEGF
angiogenesis
gemcitabine
angiotensin
pancreatic tumor
Issue Date: Aug-2009
Publisher: Spandidos Publications
Citation: Oncology Reports Vol.22 No.2 pp.355-360
Abstract: Pancreatic cancer is one of the leading causes of cancer death, and represents a challenging chemotherapeutic problem. The crucial role of angiogenesis in tumor growth has been widely recognized, and several reports have revealed that the combination treatment of the conventional chemotherapeutic drugs and anti-angiogenic agents exerted synergistic anti-cancerous effects. It has been reported that the clinically used angiotensin type-1 receptor blocker (ARB) exerted potent anti-angiogenic activity. The aim of our current study was to examine the combination effect of gemcitabine (GEM), a widely used conventional chemotherapeutic drug against pancreas cancer, and losartan (Lo), an ARB, on murine pancreatic tumor growth, especially in conjunction with angiogenesis. When used individually, GEM and Lo at clinically comparable low doses moderately suppressed pancreatic tumor development. The combination treatment with GEM and Lo exerted a marked inhibitory effect as compared with single agent treatments even after the tumor was fully established. Neovascularization and the expression of the vascular endothelial growth factor (VEGF), a central angiogenic factor, in the tumor were both markedly suppressed in a magnitude similar to the inhibitory effects against the tumor growth. Since both agents are widely used in the clinical practice, the combination regimen of GEM and Lo may represent a potential new therapeutic strategy for pancreatic cancer in the future.
URI: http://hdl.handle.net/10564/2322
ISSN: 1021335X
Appears in Collections:01111 医学科

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