This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ono, M. Articles by Sato, Y. Search for Related Content PubMed PubMed Citation Articles by Ono, M. Articles by Sato, Y.

Inhibition of Tumor Growth and Neovascularization by an Anti-Gastric Ulcer Agent, Irsogladine¹

Department of Biochemistry, Kyushu University School of Medicine, Maidashi, Higashi-ku, Fukuoka 812-82 [M. O., N. K., D. G., S. U., S. Y., H. I., M. K.]; Department of Neurosurgery, Oita Medical University, Hasama-machi, Oita 879-55 [Y. W.]; and Department of Vascular Biology, Institute of Development, Aging and Cancer, Tohoku University, Seiryo-machi, Aoba-ku, Sendai 980-77 [Y. S.], Japan

Irsogladine used clinically as an anti-gastric ulcer agent, at 10^-6–10^-4 M, inhibited cell proliferation and tubular morphogenesis of vascular endothelial cells, but the proliferation of human epidermoid cancer or glioma cells was not inhibited by this drug, even at 10^-4 M. In vivo studies demonstrated that p.o. administration of irsogladine significantly inhibited tumor growth of human glioma cells in mice, and histological analysis showed a dramatic decrease of the neovascularization in the tumors. In mice transplanted with chambers containing human glioma cells or hepatic cancer cells, irsogladine also inhibited angiogenesis. These in vivo and in vitro assays demonstrate that irsogladine may be a unique and potent inhibitor of tumor angiogenesis.

¹ This study was supported by a grant-in-aid for scientific research from the Ministry of Education, Science and Culture (Japan), the Fukuoka Anticancer Research Fund, a Yasuda Memorial Medical Grant for Cancer Research, and the Fukuoka 21th Century Medical Fund.

² To whom requests for reprints should be addressed, at Department of Biochemistry, Kyushu University School of Medicine, Maidashi, Higashi-ku, Fukuoka 812-82, Japan. Phone: 81-92-641-1151, ext. 3354 or 3355; Fax: 81-92-632-4198.

Received 12/18/95. Accepted 2/15/96.

This article has been cited by other articles:

				Y. Maruyama, M. Ono, A. Kawahara, T. Yokoyama, Y. Basaki, M. Kage, S. Aoyagi, H. Kinoshita, and M. Kuwano Tumor Growth Suppression in Pancreatic Cancer by a Putative Metastasis Suppressor Gene Cap43/NDRG1/Drg-1 through Modulation of Angiogenesis. Cancer Res., June 15, 2006; 66(12): 6233 - 6242. [Abstract] [Full Text] [PDF]

				S.-i. Ueda, Y. Basaki, M. Yoshie, K. Ogawa, S. Sakisaka, M. Kuwano, and M. Ono PTEN/Akt Signaling through Epidermal Growth Factor Receptor Is Prerequisite for Angiogenesis by Hepatocellular Carcinoma Cells That Is Susceptible to Inhibition by Gefitinib. Cancer Res., May 15, 2006; 66(10): 5346 - 5353. [Abstract] [Full Text] [PDF]

				T. Itokawa, H. Nokihara, Y. Nishioka, S. Sone, Y. Iwamoto, Y. Yamada, J. Cherrington, G. McMahon, M. Shibuya, M. Kuwano, et al. Antiangiogenic Effect by SU5416 Is Partly Attributable to Inhibition of Flt-1 Receptor Signaling Mol. Cancer Ther., March 1, 2002; 1(5): 295 - 302. [Abstract] [Full Text] [PDF]