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Tumor Biology

Abstract 370: Characterization of human umbilical vein endothelial cell clones resistant to VEGFR2 tyrosine kinase inhibitor

Kazuko Matsumoto, Tokuzo Arao, Kazuyuki Furuta, Kazuko Sakai, Tomoyuki Nagai, Kanae Kudo, Hiroyasu Kaneda, Daisuke Tamura, Keiichi Aomatsu, Yoshihiko Fujita and Kazuto Nishio
Kazuko Matsumoto
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Tokuzo Arao
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Kazuyuki Furuta
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Kazuko Sakai
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Tomoyuki Nagai
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Kanae Kudo
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Hiroyasu Kaneda
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Daisuke Tamura
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Keiichi Aomatsu
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Yoshihiko Fujita
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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Kazuto Nishio
1Kinki University School of Medicine, Osaka-Sayama, Japan.
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DOI: 10.1158/1538-7445.AM10-370 Published April 2010
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Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC

Abstract

Acquired resistance to anti-angiogenetic drugs have emerged as a potentially important problem in clinical settings, however, the underlying mechanism remains largely unclear. In this study, we established human umbilical vein endothelial cell (HUVEC) clones that are resistant to VEGFR tyrosine kinase inhibitor (VEGFR-TKI, Ki8751) using MNNG and VEGFR-TKI.

In growth inhibition assay, VEGFR-TKI resistant HUVEC clones were significantly decreased cellular sensitivity to Ki8751 about 4-10 fold compared with that in the parental cells. VEGF-mediated cellular proliferations of resistant clones were also decreased. Interestingly, VEGFR2 expression was down-regulated and the phosphorylation levels of Akt were up-regulated in resistant clones. Finally, microarray analysis revealed that several angiogenesis-related or -specific genes including CD31 were remarkably down-regulated in resistant clones compared with the parental cells. In conclusion, these results suggest that the mechanism of VEGFR-TKI resistant is closely involved in “escape phenomenon” from VEGF-VEGFR system and our findings provide a novel insight into the drug resistant to VEGFR-TKI in vascular endothelial cells.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 370.

  • ©2010 American Association for Cancer Research
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Cancer Research: 70 (8 Supplement)
April 2010
Volume 70, Issue 8 Supplement
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Abstract 370: Characterization of human umbilical vein endothelial cell clones resistant to VEGFR2 tyrosine kinase inhibitor
Kazuko Matsumoto, Tokuzo Arao, Kazuyuki Furuta, Kazuko Sakai, Tomoyuki Nagai, Kanae Kudo, Hiroyasu Kaneda, Daisuke Tamura, Keiichi Aomatsu, Yoshihiko Fujita and Kazuto Nishio
Cancer Res April 15 2010 (70) (8 Supplement) 370; DOI: 10.1158/1538-7445.AM10-370

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Abstract 370: Characterization of human umbilical vein endothelial cell clones resistant to VEGFR2 tyrosine kinase inhibitor
Kazuko Matsumoto, Tokuzo Arao, Kazuyuki Furuta, Kazuko Sakai, Tomoyuki Nagai, Kanae Kudo, Hiroyasu Kaneda, Daisuke Tamura, Keiichi Aomatsu, Yoshihiko Fujita and Kazuto Nishio
Cancer Res April 15 2010 (70) (8 Supplement) 370; DOI: 10.1158/1538-7445.AM10-370
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Cancer Research Online ISSN: 1538-7445
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