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著作: Matsumori Yuka/Yano Seiji/[後東 久嗣]/Nakataki Emiko/Wedge R. Stephen/Ryan J. Anderson/Sone Saburo/ZD6474, an inhibitor of vascular endothelial growth factor receptor tyrosine kinase, inhibits growth of experimental lung metastasis and production of malignant pleural effusions in a non-small cell lung cancer model./[Oncology Research]

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EID
235291
EOID
724531
Map
0
LastModified
2014年2月24日(月) 12:01:12
Operator
三木 ちひろ
Avail
TRUE
Censor
0
Owner
後東 久嗣
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種別 必須 学術論文(審査論文)
言語 必須 英語
招待 推奨
審査 推奨
カテゴリ 推奨
共著種別 推奨
学究種別 推奨
組織 推奨
著者 必須
  1. (英) Matsumori Yuka
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. (英) Yano Seiji
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. 後東 久嗣
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. (英) Nakataki Emiko
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. (英) Wedge R. Stephen
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. (英) Ryan J. Anderson
    役割 任意
    貢献度 任意
    学籍番号 推奨
  7. (英) Sone Saburo
    役割 任意
    貢献度 任意
    学籍番号 推奨
題名 必須

(英) ZD6474, an inhibitor of vascular endothelial growth factor receptor tyrosine kinase, inhibits growth of experimental lung metastasis and production of malignant pleural effusions in a non-small cell lung cancer model.

副題 任意
要約 任意

(英) ZD6474 is a novel, orally active inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase, with some additional activity against epidermal growth factor receptor (EGFR) tyrosine kinase. The purpose of this study was to determine the potential of ZD6474 in the control of established experimental lung metastasis and pleural effusions produced by human non-small cell lung cancer (NSCLC) cells. PC14PE6 (adenocarcinoma) and H226 (squamous cell carcinoma) cells express high levels of EGFR and only PC14PE6 cells overexpress VEGF. Neither ZD6474 nor the EGFR tyrosine kinase inhibitor gefitinib inhibit proliferation of PC14PE6 or H226 cells in vitro. Both PC14PE6 and H226 cells inoculated intravenously into nude mice induced multiple lung nodules after 5-7 weeks. In addition, PC14PE6 cells produced bloody pleural effusions. Daily oral treatment with ZD6474 did not reduce the number of lung nodules produced by PC14PE6 or H226 cells, but did reduce the lung weight and the size of lung nodules. ZD6474 also inhibited the production of pleural effusions by PC14PE6 cells. Histological analyses of lung lesions revealed that ZD6474 treatment inhibited activation of VEGFR-2 and reduced tumor vascularization and tumor cell proliferation. Therapeutic effects of ZD6474 were considered likely to be due to inhibition of VEGFR-2 tyrosine kinase because gefitinib was inactive in this model. These results indicate that ZD6474, an inhibitor of VEGFR-2, may be useful in controlling the growth of established lung metastasis and pleural effusions by NSCLC.

キーワード 推奨
  1. (英) Angiogenesis Inhibitors
  2. (英) Animals
  3. (英) Antineoplastic Agents
  4. (英) Carcinoma, Non-Small-Cell Lung
  5. (英) Cell Line, Tumor
  6. (英) Cell Proliferation
  7. (英) Endothelium, Vascular
  8. (英) Enzyme-Linked Immunosorbent Assay
  9. (英) Flow Cytometry
  10. (英) Humans
  11. 免疫組織化学(immunohistochemistry)
  12. (英) Lung Neoplasms
  13. (英) Male
  14. (英) Mice
  15. (英) Mice, Inbred BALB C
  16. (英) Neoplasm Transplantation
  17. (英) Neoplasms, Experimental
  18. (英) Neovascularization, Pathologic
  19. (英) Piperidines
  20. (英) Pleural Effusion, Malignant
  21. (英) Quinazolines
  22. (英) Receptor, Epidermal Growth Factor
  23. (英) Reverse Transcriptase Polymerase Chain Reaction
  24. (英) Vascular Endothelial Growth Factor Receptor-2
発行所 推奨
誌名 必須 Oncology Research(Cognizant Communication Corporation)
(pISSN: 0965-0407, eISSN: 1555-3906)
ISSN 任意 0965-0407
ISSN: 0965-0407 (pISSN: 0965-0407, eISSN: 1555-3906)
Title: Oncology research
Title(ISO): Oncol Res
Publisher: Cognizant Communication Corporation
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 16
必須 1
必須 15 26
都市 任意
年月日 必須 2006年 0月 初日
URL 任意
DOI 任意
PMID 任意 16783964    (→Scopusで検索)
NAID 任意
WOS 任意 000237869700002
Scopus 任意 2-s2.0-33645873707
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) Article.Affiliation: Department of Internal Medicine and Molecular Therapeutics, University of Tokushima School of Medicine, Tokushima, 3-18-15 Kuramoto-cho, Tokushima, Japan.

  2. (英) Article.PublicationTypeList.PublicationType: Journal Article