Molecular biological analysis for apoptosis induction and variation of cytoskeltons & adhesion molecules in malignant melanoma
Molecular biological analysis for apoptosis induction and variation of cytoskeltons & adhesion molecules in malignant melanoma
批准号:
12670815
负责人:
TAKAGI Hajime
金额:
$2.56万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2000
资助国家:
日本
项目状态:
已结题
起止时间:
2000 至 2001
中文摘要
基本research1。免疫组织化学证实序贯生物免疫化疗诱导小鼠黑色素瘤细胞凋亡。2. 通过FACScan检测培养的人黑色素瘤细胞的药物敏感性。3. 免疫荧光技术检测细胞骨架的变化,特别是波形蛋白的变化。但由于技术上的问题,分析是不够的。4. 没有进行动物实验。我们没有准备好迎接一个有利的环境。5. 我们比较了化疗前后多药耐药相关蛋白的程度。6. 我们一直在尝试建立耐药黑色素瘤细胞细胞系。临床research1。我们采用免疫组化方法研究黑色素瘤患者标本中的凋亡细胞、凋亡相关基因/蛋白和粘附分子。2. 采用酶联免疫吸附法测定黑素瘤抑制活性,并检查其价值与临床病程的相关性。3. 我们评估了晚期恶性黑色素瘤的联合化疗(DAC-Tam)。在这段时间里我们不能展示足够的成果,但是我们有一些很有前景的产品。我们将继续这个项目进行一些实验。
英文摘要
Basic research1. Immunohistochemically we confirmed sequential bioimmunochemotherapy induced apoptosis for mouse melanoma cells. 2. We checked drug sensitivity of cultured human melanoma cells by FACScan. 3. Variation of cytoskelton, especially vimentin, were examined with immunofluorescent technique. But analysis was not enough, because of technical trouble. 4. Animal experiments were not done. We did not prepare to a favorable environment. 5. We compared extent of multidrug-resistance-associated protein between before and after chemotherapy. 6. We have been trying establish cell line of drug resistant melanoma cells.Clinical research1. We refer to the apoptosis cells, apoptosis- related gene/protein, and adhesion molecules by melanoma patients specimens immunohistochemically. 2. We measured melanoma inhibitory activity by ELISA method, and checked with association of the value and clinical course. 3. We evaluated of combination chemotherapy (DAC-Tam) for advanced malignant melanoma.SummaryWe cannot show enough results in this periods, but we got some promising products. We will keep this projects going on some experiments.
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Kubo H, Matsumoto K, Funahashi M, Takagi H, Kitajima Y, Taniguchi S and Saida T: "Sequential chemoimmunotherapy with cisplatin, interferon-beta and interleukin-2 inhibits the growth of B16-F1 melanoma in cyngeneic mice"Melanoma Research. 10. 223-229 (2000
Kubo H、Matsumoto K、Funahashi M、Takagi H、Kitajima Y、Taniguchi S 和 Saida T:“使用顺铂、干扰素-β 和白细胞介素 2 的序贯化学免疫疗法抑制新生小鼠中 B16-F1 黑色素瘤的生长”黑色素瘤研究。
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Kamiya H, Kanoh H, Ichihashi N, Ichiki Y, Takagi H, and Kitajima Y: "Evaluations of combination chemotherapy (DAC-Tam) for advanced malignant melanoma"Nishinihon J Dermatol. 63. 561-568 (2002)
Kamiya H、Kanoh H、Ichihashi N、Ichiki Y、Takagi H 和 Kitajima Y:“晚期恶性黑色素瘤联合化疗 (DAC-Tam) 的评估”Nishinihon J Dermatol。
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神谷秀喜他: "進行期悪性黒色腫に対するDAC-Tam 療法の使用経験"西日皮膚. 63. 561-568 (2001)
Hideki Kamiya 等人:“DAC-Tam 治疗晚期恶性黑色素瘤的经验”Nishinichi Skin 63. 561-568 (2001)。
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H.Kubo et al.: "Sequential chemoimmuno therapy with cisplatin, interferon-β and interleukin-2 inhibits the growth of B16-F1 melanoma in syngeneic mice"Melanoma Research. 10. 223-229 (2000)
H. Kubo 等人:“使用顺铂、干扰素-β 和白介素-2 的序贯化学免疫疗法抑制同系小鼠中 B16-F1 黑色素瘤的生长”Melanoma Research 10. 223-229 (2000)。
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Molecular Biological Analysis for the Role of Plasminogen Activator in Wound Healings
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批准号:08670959
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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:1996
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负责人:TAKAGI Hajime
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依托单位: