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著作: [井本 逸勢]/Tsuda Hitoshi/Hirasawa Akira/Miura Masahiko/Sakamoto Masaru/Hirohashi Setsuo/Inazawa Johji/Expression of cIAP1, a target for 11q22 amplification, correlates with resistance of cervical cancers to radiotherapy./[Cancer Research]

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EID
226137
EOID
1002785
Map
0
LastModified
2021年3月18日(木) 11:09:53
Operator
三木 ちひろ
Avail
TRUE
Censor
0
Owner
[副研究部長]/[徳島大学.大学院医歯薬学研究部]
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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 研究
共著種別 推奨
学究種別 推奨
組織 推奨
著者 必須
  1. 井本 逸勢
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. (英) Tsuda Hitoshi
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. (英) Hirasawa Akira
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. (英) Miura Masahiko
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. (英) Sakamoto Masaru
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. (英) Hirohashi Setsuo
    役割 任意
    貢献度 任意
    学籍番号 推奨
  7. (英) Inazawa Johji
    役割 任意
    貢献度 任意
    学籍番号 推奨
題名 必須

(英) Expression of cIAP1, a target for 11q22 amplification, correlates with resistance of cervical cancers to radiotherapy.

副題 任意
要約 任意

(英) Inhibition of, or increased resistance to, apoptosis is a common property of cancer cells. This means that a constitutive activation of antiapoptotic molecules via genetic or epigenetic mechanisms, including gene amplification, may well be involved in carcinogenesis. Recently we reported that cIAP1, an inhibitor of apoptosis, is overexpressed through 11q22 amplification in cell lines derived from esophageal squamous cell carcinomas and is associated with resistance of esophageal squamous cell carcinomas to drug-induced apoptosis (I. Imoto et al. Cancer Res., 61: 6629-6634, 2001). Because amplification of 11q22 has been implicated in other malignancies also, including cervical squamous cell carcinomas (CSCCs), we attempted to correlate amplification and overexpression of cIAP1 with radiation sensitivity in CSCC-derived cell lines and primary CSCC tumors. In the nine cell lines we examined, two showed amplification and consistent overexpression of cIAP1, as well as significant resistance to radiation-induced cell death as compared with lines showing no cIAP1 amplification. Immunohistochemical analysis of 70 primary CSCCs from patients treated only with radiotherapy demonstrated that both overall survival and local recurrence-free survival was significantly poorer among patients with tumors showing high levels of nuclear cIAP1 staining than among patients whose tumors revealed little or no nuclear cIAP1. Multivariate analysis showed nuclear cIAP1 staining to be an independent predictive factor for local recurrence-free survival after radiotherapy among patients with CSCC. These findings demonstrate that cIAP1 may play an important role in the development/progression of this disease and that cIAP1 could be a novel predictive marker for resistance to radiotherapy in individual CSCC patients.

キーワード 推奨
  1. (英) Adult
  2. (英) Aged
  3. (英) Aged, 80 and over
  4. (英) Carcinoma, Squamous Cell
  5. 細胞死(cell death)
  6. (英) Chromosomes, Human, Pair 11
  7. 女性(female)
  8. (英) Gene Amplification
  9. (英) Humans
  10. 免疫組織化学(immunohistochemistry)
  11. (英) Inhibitor of Apoptosis Proteins
  12. (英) Middle Aged
  13. (英) Neoplasm Staging
  14. (英) Protein Biosynthesis
  15. (英) Proteins
  16. (英) Radiation Tolerance
  17. (英) Survival Rate
  18. (英) Tumor Cells, Cultured
  19. (英) Uterine Cervical Neoplasms
発行所 推奨
誌名 必須 Cancer Research(American Assotiation for Cancer Research)
(pISSN: 0008-5472, eISSN: 1538-7445)
ISSN 任意 0008-5472
ISSN: 0008-5472 (pISSN: 0008-5472, eISSN: 1538-7445)
Title: Cancer research
Title(ISO): Cancer Res
Publisher: American Association for Cancer Research
 (NLM Catalog  (Scopus  (Scopus  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 62
必須 17
必須 4860 4866
都市 任意
年月日 必須 2002年 9月 1日
URL 任意
DOI 任意
PMID 任意 12208731    (→Scopusで検索)
NAID 任意
WOS 任意 000177897200004
Scopus 任意
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) Affiliation: Department of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical & Dental University, Tokyo 113-8510, Japan.

  2. (英) PublicationType: Journal Article

  3. (英) PublicationType: Research Support, Non-U.S. Gov't