Investigation of Biological Behavior and Treatment Modality for Ovarian Clear Cell Adenocarcinoma
Investigation of Biological Behavior and Treatment Modality for Ovarian Clear Cell Adenocarcinoma
批准号:
09671667
负责人:
FUJIMURA Masaki
金额:
$1.86万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 2000
中文摘要
发现治疗卵巢透明细胞腺癌(CCA)的基本抗癌药物是cpt - 1。热疗和添加甘油被认为是抗癌药物的增强剂,但对其临床有效状况的影响不足。雌激素受体-α (ER α)和ER β在临床切除的卵巢CCA标本和培养的ccac细胞系中均无表达。EGF-R被认为位于ERα的下游,通过EGF-R刺激EOF和TGF α,通过自倾斜系统刺激CCA细胞株的生长和侵袭。通过HER2的刺激也参与了卵巢CCA细胞系的生长。易瑞沙(Iressa)是一种特异性的EGF-R磷酸化抑制剂,可以剂量依赖性地抑制CCA细胞系的生长和侵袭。易瑞沙还能抑制SCID小鼠背部异种移植CCA(rmg - 1)的生长。给予易瑞沙的小鼠比对照组小鼠存活时间更长。Herceptin被称为人源抗her2单克隆抗体,在体外和体内也能抑制CCA细胞株的生长。服用赫赛汀的小鼠比对照组存活时间更长。由此可见,易瑞沙和赫赛汀是CCA细胞系的有效抑制剂,可作为CCA临床综合治疗方式之一。
英文摘要
The basic anti-caner drug for treating ovarian clear cell adenocarcinoma (CCA) was revealed to be CPT-ll. Hyperthermia and Glycerol addition which were known as enhencer of anti-cancer drug, have insufficient effect on its clinically available condition. Estrogen receptor-α (ER α), and ER β were not expressed in clinically resected Ovarian CCA specimens and cultured CCAcell lines. EOF and TGF α stimulation through EGF-R, which was thought to be located at the lower stream of ERα, stimulated the growth and invasion of CCA cell lines by autocline system. Stimulation through HER2 was also involved in the growth of ovarian CCA cell lines. Then Iressa, a specific inhibitor of EGF-R phosphorylation, inhibited the growth and invasion of CCA cell lines dose dependently. Iressa also inhibit the growth of xenografted CCA(RMG-l) on the back of SCID mice. The mice in which Iressa was administered survived more longer than the mice in control group. Herceptin which is known as humanized anti-HER2 monoclonal antibody, also inhibited the growth of CCA cell line in vitro and in vivo. Also Herceptin administered mice survived more longer than the mice in control group.From these findings, Iressa and Herceptin were revealed to be potent inhibitors of CCA cell lines and could be a good candidate as one of clinically comprehensive treatment modality for CCA.
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Fujimura M., Hidaka T., Kataoka K, Yamakawa Y., Akada S., Teranishi A. and Saito S.: "Absence of estrogen receptor-α expression in human ovarian clear cell adenocarcinoma compared with ovarian serous, endometrioid, and mucinous adenocarcinoma."Am. J. Surg
Fujimura M.、Hidaka T.、Kataoka K、Yamakawa Y.、Akada S.、Teranishi A. 和 Saito S.:“与卵巢浆液性、子宫内膜样和粘液性腺癌相比,人卵巢透明细胞腺癌中缺乏雌激素受体-α 表达“腺癌。”J. Surg。
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Fujimura M., Hidaka T., Saito S.: "Selective inhibition of the epidermal growth factor receptor by ZD1839 ('IRESSA') decreses the growth and invasion of ovarian clear cell adenocarcinoma cells"Clin. Cancer Res.. (in press).
Fujimura M.、Hidaka T.、Saito S.:“ZD1839(‘易瑞莎’)选择性抑制表皮生长因子受体可减少卵巢透明细胞腺癌细胞的生长和侵袭”Clin。
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藤村正樹, 片岡 健, 日高隆雄, 斎藤 滋: "卵巣明細胞腺癌における抗癌剤感受性試験"Oncology & Chemotherapy. 16. 241-244 (2000)
Masaki Fujimura、Ken Kataoka、Takao Hidaka、Shigeru Saito:“卵巢透明细胞腺癌的抗癌药物敏感性测试”《肿瘤学与化疗》16. 241-244 (2000)。
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Fujimura M, Hidaka T, Saito S: "Selective inhibition of the epidermal growth factor receptor by ZD1839 ('IRESSA') decreses the growth and invasion of ovarian clear cell adenocarcinoma cells"Clin Cancer Res. (in press).
Fujimura M、Hidaka T、Saito S:“ZD1839(‘易瑞莎’)选择性抑制表皮生长因子受体可减少卵巢透明细胞腺癌细胞的生长和侵袭”Clin Cancer Res。
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Fujimura M.,Yamakawa Y.,Kataoka K. et al.: "Preservation of the vulva in stage III squamous cell carcinoma with intra-arterial chemotherapy."Int.J.Clin.Oncol.. 4. 307-310 (1999)
Fujimura M.、Yamakawa Y.、Kataoka K. 等人:“通过动脉内化疗保留 III 期鳞状细胞癌的外阴。”Int.J.Clin.Oncol.. 4. 307-310 (1999)
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共 8 条
To overcome intractable chronic cough: disclosure of mechanism of cough response to bronchoconstiction to conrol of the cough
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批准号:23591142
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$3.24万
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财政年份:2011
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负责人:FUJIMURA Masaki
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依托单位:
To overcome the intractable chronic cough : mechanism of cough and development of therapy
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批准号:20590916
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.91万
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财政年份:2008
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负责人:FUJIMURA Masaki
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依托单位:
Importance of environmental fungi and IgE non-mediated mechanism in atopic eough
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批准号:17607003
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.53万
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财政年份:2005
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负责人:FUJIMURA Masaki
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依托单位:
DEVELOPMENT OF DIAGNOSIS AND TREATMENT BASED ON PATHOPHYSIOLOGY OF CHRONIC COUGH
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批准号:14570546
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.18万
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财政年份:2002
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负责人:FUJIMURA Masaki
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依托单位:
Involvement of Enteric Nervous System in the Regulation of Gastrointestinal Motility
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批准号:07671384
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.34万
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财政年份:1995
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负责人:FUJIMURA Masaki
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依托单位:
Pathophysiology of specific bronchial hyperresponsiveness
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批准号:07670662
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.6万
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财政年份:1995
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负责人:FUJIMURA Masaki
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依托单位:
Mechanisms of heightened airway cough receptor sensitivity in eosinophilic bronchitis (atopic cough : eosinophilic bronchitis without asthma).
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批准号:04807055
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.28万
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财政年份:1992
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负责人:FUJIMURA Masaki
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依托单位:
海外基金